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Drying-rewetting (DW) cycles can significantly influence soil properties and microbial community composition, leading to direct or indirect changes in arsenic (As) toxicity, which inturn affects soil ecological functions. Despite this, there has been insufficient focus on accurately evaluating As ecotoxicity and its impact on soil ecological function under DW conditions. This study seeks to address this gap by examining the effects of DW on As toxicity and the characteristics of soil ecological function, specifically from the perspective of enzyme-based functional diversity. Our results reveal that compared to constant moisture conditions, DW treatment significantly increased the toxicity of As on alkaline phosphatase and β-glucosidase, with maximum inhibition rates observed at 46.29% and 21.54%, respectively. Conversely, for other tested enzymes including invertase, fluorescein diacetate hydrolase, and dehydrogenase, DW treatment decreased As toxicity, possibly be due to the different stability of these enzymes under varying soil moisture conditions. From an enzyme functional diversity perspective, DW treatment reduced the As toxicity, as evidenced by the reduced inhibition rates and a lower coefficient of variation. In conclusion, DW appears to enhance soil functional resilience against arsenic pollution. These findings contribute to a better understanding of changes in ecological functions in heavy metal-contaminated soils under dynamic environmental conditions, offering insights for improved monitoring and mitigation strategies for metalloids toxicity in natural environments., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Ltd. All rights reserved.)

Severe toxic effects of arsenic on human physiology have been of immense concern worldwide. Arsenic causes irrevocable structural and functional disruption of tissues, leading to major diseases in chronically exposed individuals. However, it is yet to be resolved whether the effects result from direct deposition and persistence of arsenic in tissues, or via activation of indirect signaling components. Emerging evidences suggest that gut inhabitants play an active role in orchestrating various aspects of brain physiology, as the gut-brain axis maintains cognitive health, emotions, learning and memory skills. Arsenic-induced dysbiosis may consequentially evoke neurotoxicity, eventually leading to anxiety and depression. To delineate the mechanism of action, mice were exposed to different concentrations of arsenic. Enrichment of Gram-negative bacteria and compromised barrier integrity of the gut enhanced lipopolysaccharide (LPS) level in the bloodstream, which in turn elicited systemic inflammation. Subsequent alterations in neurotransmitter levels, microglial activation and histoarchitectural disruption in brain triggered onset of anxiety- and depression-like behaviour in a dose-dependent manner. Finally, to confirm whether the neurotoxic effects are specifically a consequence of modulation of gut microbiota (GM) by arsenic and not arsenic accumulation in the brain, fecal microbiota transplantations (FMT) were performed from arsenic-exposed mice to healthy recipients. 16S rRNA gene sequencing indicated major alterations in GM population in FMT mice, leading to severe structural, functional and behavioural alterations. Moreover, suppression of Toll-like receptor 4 (TLR4) using vivo-morpholino oligomers (VMO) indicated restoration of the altered parameters towards normalcy in FMT mice, confirming direct involvement of the GM in inducing neurotoxicity through the arsenic-gut-brain axis. This study accentuates the potential role of the gut microbiota in promoting neurotoxicity in arsenic-exposed mice, and has immense relevance in predicting neurotoxicity under altered conditions of the gut for designing therapeutic interventions that will target gut dysbiosis to attenuate arsenic-mediated neurotoxicity., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Ltd. All rights reserved.)

Selenium (Se) fortification is witnessed to simultaneously inhibit absorbing Cadmium (Cd) and Arsenic (As) by rice plants, but the mechanism is unclear. Here, the effects of Se on the root morphology, iron plaque (IP) content, soil Fe 2+ content, radial oxygen loss (ROL), and enzyme activities of the rice plants in the soil contaminated by Cd and As were intensively investigated through the hydroponic and soil experiments. Se effectively alleviated the toxic effects of Cd and As on the plants and the dry weight, root length, and root width were increased by 203.18%, 33.41%, and 52.81%, respectively. It also elucidated that ROL was one of the key factors to elevate IP formation by Se and the specific pathways of Se enhancing ROL were identified. ROL of the plants in the experiment group treated by Se was increased 36.76%, and correspondingly IP was magnified 50.37%, compared to the groups with Cd and As. It was owing to Se significantly increased the root porosity (62.11%), facilitating O 2 transport to the roots. Additionally, Se enhanced the activities of catalase (CAT) and superoxide dismutase (SOD) to promote the catalytic degradation of ROS induced by Cd and As stress. It indirectly increased O 2 release in the rhizosphere, which benefit to form more robust IP serve as stronger barrier to Cd and As. The results of our study provide a novel molecular level insight for Se promoting root IP to block Cd and As uptake by the rice plants., Competing Interests: Declaration of competing interest We declare that we do not have any commercial or associative interest that represents a conflict of interest in connection with the work submitted., (Copyright © 2024 Elsevier Ltd. All rights reserved.)

The assessment of human health risk due to the presence of hazardous elements in the environment is now necessary for environmental management and legislative initiatives. This study aims to determine the contamination by As, Cd, Pb, and Cr in soils near gold mines in three municipalities located in the Andean region of Colombia. One of the main objectives of the study is to explore possible correlations between the Lifetime Cancer Risk (LCR) and phytotoxicity biomarkers using a simple and rapid-response plant model, radish (Raphanus sativus L.). In the municipality of Yalí, Puerto Berrío, and Buriticá, the hazardous elements concentrations ranged from 8.1 to 35.5, 1.7 to 892, and 5.8 to 49.8 for As, 0.1 to 4.6, 0.1 to 65.2, and 0.5 to 18.2 for Cd, 18.5 to 201.3, 13.0 to 1908, and 189 to 2345 for Pb, and 5.4 to 118.4, 65.4 to 301, and 5.4 to 102.3 for Cr, respectively. The results showed that the biomarkers intracellular H 2 O 2 concentration, antioxidant activity, and radicle elongation exhibited significant (P < 0.05) variations associated with the concentration of hazardous elements in the soils. Significant correlations (P < 0.05, r > 0.58) were found between the biomarkers and the LCR for Cd, Pb, and Cr, but not for As. The results using biomarkers reveal that soil pH and organic matter content are important variables that control the bioavailability of these elements in the soil. The use of indicators like LCR alone has limitations and should be accompanied by the use of biomarkers that allow for a better understanding of the biological system's response to exposure to potentially toxic elements. The results obtained show the urgent need to implement public policies to minimize exposure to hazardous substances in areas near gold mining projects., Competing Interests: Declaration of competing interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests:Julián E. López reports financial support was provided by Institución Universitaria Colegio Mayor de Antioquia. If there are other authors, they declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024. Published by Elsevier Ltd.)

The modified biochars have positive effects in reducing heavy metal toxicity for plants. However, the mechanism and extent of these effects on mitigating arsenic toxicity and plant performance are not clear. Thus, a pot experiment was conducted as factorial to evaluate the potential of fresh and enriched biochars with potassium and magnesium nano-sulfates [potassium-enriched biochar (K-BC), magnesium-enriched biochar (Mg-BC) in individual and combined forms] on reducing arsenic toxicity (non-contamination, 50, and 100 mg NaAsO 2 kg -1 soil) in basil plants. Biochar-related treatments reduced plant arsenic absorption rate (up to 24%), arsenic content of root (up to 38%) and shoot (up to 21%) and root tonoplast H + -ATPase activity (up to 30%). The fresh and particularly enriched biochars improved soil properties (pH, CEC, and available iron content), ferric chelate reductase activity, iron, potassium and magnesium contents of plant tissues, chlorophyll content index, photochemical efficiency of photosystem II, relative electron transport rate, leaf area, and basil growth (shoot and root dry weight). These results revealed that enriched biochars are useful soil amendments for improving physiological performance of plants via reducing heavy metal toxicity and enhancing cation exchange capacity, nutrient availability and ferric chelate reductase activity. Therefore, soil amendment by enriched biochars could be a sustainable solution for enhancing plant productivity in contaminated soils via mitigating environmental impacts. This is an environmentally friendly method for using the natural wastes to overcome the adverse effects of soil pollutants on medicinal plants., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Ltd. All rights reserved.)

This study explored the effect of a toxic metal(oid) mixture (cadmium, lead, arsenic, mercury, chromium, and nickel) on thyroid function in Wistar rats exposed for 28 or 90 days. Dose levels were determined based on prior human-biomonitoring investigation. The experiment included control (male/female rats, 28 and 90 days) and treated groups, reflecting the lower confidence limit of the Benchmark Dose (BMDL) for hormone levels (M1/F1, 28 and 90 days), median concentrations (M2/F2, 28 and 90 days), 95th percentile concentrations (M3/F3, 28 and 90 days) measured in a human study, and reference values for individual metals extracted from the literature (M4/F4, 28 days only). Blood and thyroid gland samples were collected at the experimental termination. Serum TSH, fT3, fT4, T3, and T4 levels were measured, and SPINA-GT and SPINA-GD parameters were calculated. In silico analysis, employing the Comparative Toxicogenomic Database and ToppGene Suite portal, aimed to reveal molecular mechanisms underlying the observed effects. Results showed greater sensitivity in the female rats, with significant effects observed at lower doses. Subacute exposure increased TSH, fT3, and T3 levels in females, while subchronic exposure in males decreased TSH and fT3 levels and increased fT4. Subacute exposure induced changes even at allegedly safe doses, emphasizing potential health risks. Histological abnormalities were observed in all the treated groups. In silico findings suggested that toxic metal exposure contributes to thyroid disorders via oxidative stress, disruption of micronutrients, interference with hormone synthesis, and gene expression dysregulation. These results indicate that seemingly safe doses in single-substance research can adversely affect thyroid structure and function when administered as a mixture. These findings highlight the complex impact of toxic metal exposure on thyroid health, emphasizing that adhering to accepted safety limits for single-substance research fails to account for adverse effects on thyroid structure and function upon exposures to metal mixtures., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Ltd. All rights reserved.)

We previously reported the neurotoxic effects of arsenic in the hippocampus. Here, we explored the involvement of Wnt pathway, which contributes to neuronal functions. Administering environmentally relevant arsenic concentrations to postnatal day-60 (PND60) mice demonstrated a dose-dependent increase in hippocampal Wnt3a and its components, Frizzled, phospho-LRP6, Dishevelled and Axin1 at PND90 and PND120. However, p-GSK3-β(Ser9) and β-catenin levels although elevated at PND90, decreased at PND120. Additionally, treatment with Wnt-inhibitor, rDkk1, reduced p-GSK3-β(Ser9) and β-catenin at PND90, but failed to affect their levels at PND120, indicating a time-dependent link with Wnt. To explore other underlying factors, we assessed epidermal growth factor receptor (EGFR) pathway, which interacts with GSK3-β and appears relevant to neuronal functions. We primarily found that arsenic reduced hippocampal phosphorylated-EGFR and its ligand, Heparin-binding EGF-like growth factor (HB-EGF), at both PND90 and PND120. Moreover, treatment with HB-EGF rescued p-GSK3-β(Ser9) and β-catenin levels at PND120, suggesting their HB-EGF/EGFR-dependent regulation at this time point. Additionally, rDkk1, LiCl (GSK3-β-activity inhibitor), or β-catenin protein treatments induced a time-dependent recovery in HB-EGF, indicating potential inter-dependent mechanism between hippocampal Wnt/β-catenin and HB-EGF/EGFR following arsenic exposure. Fluorescence immunolabeling then validated these findings in hippocampal neurons. Further exploration of hippocampal neuronal survival and apoptosis demonstrated that treatment with rDkk1, LiCl, β-catenin and HB-EGF improved Nissl staining and NeuN levels, and reduced cleaved-caspase-3 levels in arsenic-treated mice. Supportively, we detected improved Y-Maze and Passive Avoidance performances for learning-memory functions in these mice. Overall, our study provides novel insights into Wnt/β-catenin and HB-EGF/EGFR pathway interaction in arsenic-induced hippocampal neurotoxicity., Competing Interests: Declaration of competing interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests:Asmita Garg reports financial support was provided by University Grants Commission, Gov. of India., (Copyright © 2024 Elsevier Ltd. All rights reserved.)

Developmental exposure to environmental pollutants has been shown to promote adverse health outcomes in offspring. Exposure to heavy metals such as arsenic which also has endocrine-disrupting activity is being increasingly linked with cancers, diabetes, and lately with Metabolic Syndrome (MetS). In this work, we have assessed the effects of preconceptional plus gestational arsenic exposure on the developmental programming of MetS in offspring. In our study, only gestational arsenic exposure led to reduced birth weight, followed by catch-up growth, adiposity, elevated serum triglycerides levels, and hyperglycemia in male offspring. Significant adipocyte dysfunction was observed in offspring with increased hypertrophy, insulin resistance, and chronic inflammation in epididymal white adipose tissue. Adipose tissue regulates the metabolic health of individuals and its dysfunction resulted in elevated serum levels of metabolism-regulating adipokines (Leptin, Resistin) and pro-inflammatory cytokines (PAI-1, TNFα). The progenitor adipose-derived stem cells (AdSCs) from exposed progeny had increased proliferation and adipogenic potential with excess lipid accumulation. We also found increased activation of Akt, ERK1/2 & p38 MAPK molecules in arsenic-exposed AdSCs along with increased levels of phospho-Insulin-like growth factor-1 receptor (p-IGF1R) and its upstream activator Insulin-like growth factor-2 (IGF2). Overexpression of Igf2 was found to be due to arsenic-mediated DNA hypermethylation at the imprinting control region (ICR) located -2kb to -4.4 kb upstream of the H19 gene which caused a reduction in the conserved zinc finger protein (CTCF) occupancy. This further led to persistent activation of the MAPK signaling cascade and enhanced adipogenesis leading to the early onset of MetS in the offspring., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Ltd. All rights reserved.)

This study investigates our hypothesis that how effect of arsenic stress on okra (Abelmoschus esculentus L.) can be alleviated through the use of waste materials such as steel slag (SS) and corncob biochar (BC). Different growth variables, biochemical parameters, oxidative stress markers, enzymatic and non-enzymatic antioxidants and glyoxylase enzyme activities were assessed. When okra was exposed to As, there was a noticeable decrease in seedling length, biomass, relative water content, various biochemical attributes, however, electrolyte leakage and lipid peroxidation in okra were enhanced. The supplementation of SS and BC-either individually or in combination-improved the growth parameters and reduced oxidative stress markers. Application of SS and BC also lowered As accumulation in roots and shoots of okra mitigating adverse effects of As exposure. Additionally, the activities of antioxidant and glyoxalase enzyme increased when SS and BC were present, concurrently reducing methylglyoxal content. Arsenic-induced stress led to oxidative damage, an enhancement in both enzymatic and non-enzymatic antioxidants, induced the synthesis of thiol and phytochelatins in roots and shoots. These may play a vital function in alleviating oxidative stress induced by As. Superoxide dismutase, catalase, ascorbate peroxidase, and glutathione reductase activities were significantly enhanced in As-treated plants. These enhancement were further amplified when SS and BC were amended to As-treated okra. Therefore, synergistic application of SS and BC effectively protects okra against oxidative stress induced by As by increasing both antioxidant defense and glyoxalase systems. Both SS, an industrial byproduct, and BC, generated from agricultural waste, are cost-effective, environmentally friendly, safe, and non-toxic materials which can be used for crop production in As contaminated soil., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Ltd. All rights reserved.)

Arsenic, as a metalloid, has the ability to move and transform in different environmental media. Its widespread contamination has become a significant environmental problem and public concern. Arsenic can jeopardize multiple organs through various pathways, influenced by environmental bioprocesses. This article provides a comprehensive overview of current research on the cardiovascular hazards of arsenic. A bibliometric analysis revealed that there are 376 papers published in 145 journals, involving 40 countries, 631 institutions, and 2093 authors, all focused on arsenic-related concerns regarding cardiovascular health. China and the U.S. have emerged as the central hubs of collaborative relationships and have the highest number of publications. Hypertension and atherosclerosis are the most extensively studied topics, with redox imbalance, apoptosis, and methylation being the primary mechanistic clues. Cardiovascular damage caused by arsenic includes arrhythmia, cardiac remodeling, vascular leakage, and abnormal angiogenesis. However, the current understanding is still inadequate over cardiovascular impairments, underlying mechanisms, and precautionary methods of arsenic, thus calling an urgent need for further studies to bridge the gap between environmental processes and arsenic hazards., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Ltd. All rights reserved.)

Globally freshwater ecosystems and associated biota including phytoplankton communities are at extreme risk from trace metal pollution originating from geogenic as well as from anthropogenic sources such as release of untreated industrial effluents. In the present study influence of iron- and arsenic-enrichments on structure and metabolism of phytoplankton communities of River Ganga, one of the largest rivers of South Asia, was assessed under laboratory-based microcosm experiments. Surface water samples were collected and subsequently enriched with higher than recommended concentrations of iron (10 mg/L) and arsenic (10 μg/L). The set-up comprised of nine containers of 25 L volume with three containers each for iron- and arsenic-enrichment and was maintained for 30 days. Trace metal enrichment rapidly changed the phytoplankton community structure and chemistry of nutrients uptake. Iron-enrichment prompted diatom blooms comprising of Thalassiosira, succeeded by green algae Coelastrum. Arsenic-enrichment maintained cyanobacteria for longer time-spans compared to the control and iron-enriched containers but significantly lesser abundance of diatoms. Variations in community composition was also reflected in nutrient uptake rates with silicate release in the arsenic-enriched containers at the end of the experiment. Changes in macronutrient dynamics also altered genus growth rates wherein both iron- and arsenic appeared to lower the death rate of Thalassosira but stimulated growth of other genera including Skeletonema and Pandorina. Iron appeared to influence lesser number of genera compared to arsenic which altered growth rates of both diatoms and green algae. This consequently influenced the gross primary productivity values which lowered both in the iron- and arsenic-enriched containers compared to the control owing to decrease in phytoplankton diversity. Iron appeared to drive phytoplankton communities toward a less general and more specialized composition with high abundance of selective species comprising of small diatoms such as Thalassiosira, whereas arsenic appears to select for green algal enrichment in freshwater ecosystems., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier Ltd. All rights reserved.)

Abstract Chronic exposure to high levels of arsenic is closely associated with nervous system disorders that harm learning, memory, and intelligence. Studies have shown that the primary characteristic of brain damage is neuronal apoptosis. Arsenic induces apoptosis in a variety of nerve cells. Therefore, substance that inhibit apoptosis promise to mitigate arsenic toxicity. Pigment epithelium-derived factor (PEDF) is widely distributed in brain tissues and has various effects on neurons, including induction of apoptosis. Our previous study suggested that PEDF might augment arsenic-induced apoptosis in rat brains. In this study of 151 adults with normal, mild, moderate, and high exposure to arsenic, the measured serum PEDF levels were 15.46 ± 5.87 ng/mL, 17.33 ± 8.22 ng/mL, 19.43 ± 9.51 ng/mL and 21.65 ± 14.46 ng/mL, respectively. Multiple linear regression analysis revealed an independent positive correlation between serum PEDF levels and arsenic exposure in drinking water. To study the underlying mechanism of arsenic-induced apoptosis, we exposed PEDF-transfected PC12 cells to NaAsO 2. We discovered that NaAsO 2- -induced mitochondrial apoptosis was enhanced in cells that over expressed PEDF. Moreover, p53 up regulated modulator of apoptosis (PUMA) gene and B-cell lymphoma 2 (Bcl-2) protein were primary factors in the progression of arsenic-induced apoptosis. Taken together, our results suggest that PEDF inhibition might mitigate arsenic toxicity to nerve cells. Graphical abstract Image Highlights • PEDF level in serum is positively correlated with arsenic exposure in drinking water. • PEDF promoted the mitochondrial apoptosis of nerve cells. • PEDF promoted the mitochondrial apoptosis induced by arsenic. [ABSTRACT FROM AUTHOR]

Metal contamination poses a significant threat to elasmobranchs, underscoring the need for targeted conservation approaches. The critically endangered Brazilian guitarfish, Pseudobatos horkelii, confronts an array of challenges, notably overexploitation, putting its survival at risk. Our study investigated the potential toxicity arising from arsenic (As), cadmium (Cd), mercury (Hg), and lead (Pb) contamination across various adult guitarfish tissues from southeastern Brazil. Serological stress indicators, nutritional metabolites, and creatinine, an organ function marker, were also assessed, and Selenium (Se) levels were also investigated for possible protective effects. Our investigation unveiled significant correlations between metal concentrations and the determined physiological markers, shedding light on potential adverse effects. Remarkably, six correlations were indicative of how Hg and Pb negatively impact hepatic metabolite assimilation, while As was shown to influence renal phosphorus dynamics, Cd to affect rectal gland phosphorus regulation, and Pb to influence creatinine production in muscle tissue. Furthermore, Se demonstrated protective properties against Cd, Hg, and Pb, suggesting a role in alleviating the toxicity of these elements. Despite probable protective Se influences, the detected elemental interactions still suggest potential for organ impairment. These findings gain heightened significance within the context of the cumulative stressors faced by the Brazilian guitarfish, with metal contamination exhibiting the capacity to erode this species resilience against both anthropogenic and environmental pressures, thereby disrupting systemic equilibrium and jeopardizing wild populations. By investigating the intricate balance between metal accumulation and physiological consequences, our study contributes with crucial insights into potential conservation strategy formulations towards pollution for this critically endangered elasmobranch species., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier Ltd. All rights reserved.)

Zinc oxide nanoparticles (nZn) have emerged as vital agents in combating arsenic (As) stress in plants. However, their role in mitigation of As induced oxidative stress is less studied. Therefore, this study aimed to assess the comparative role of nZn and ZnO in alleviating As toxicity in rice genotype "9311". The results of this study revealed that nZn demonstrated superior efficacy compared to ZnO in mitigating As toxicity. This superiority can be attributed to the unique size and structure of nZn, which enhances its ability to alleviate As toxicity. Exposure to As at a concentration of 25 μM L -1 led to significant reductions in shoot length, root length, shoot dry weight, and root dry weight by 39%, 51%, 30%, and 46%, respectively, while the accumulation of essential nutrients such as magnesium (Mg), potassium (K), iron (Fe), manganese (Mn), and zinc (Zn) decreased by 25%-47% compared to the control plants. Additionally, As exposure resulted in stomatal closure and structural damage to vital cellular components such as grana thylakoids (GT), starch granules (SG), and the nucleolus. However, the application of nZn at a concentration of 30 mg L -1 exhibited significant alleviation of As toxicity, resulting in a reduction of As accumulation by 54% in shoots and 62% in roots of rice seedlings. Furthermore, nZn demonstrated the ability to scavenge reactive oxygen species (ROS) like hydrogen peroxide (H 2 O 2 ) and superoxide anion (O 2 .- ), while significantly promoted the gas exchange parameters, chlorophyll content (SPAD value), fluorescence efficiency (Fv/m) and antioxidant enzyme activities under As-induced stress. These findings highlight the potential of nZn in mitigating the adverse impacts of As contamination in rice plants. However, further research is necessary to fully comprehend the underlying mechanisms responsible for the protective effects of nZn and to determine the optimal conditions for their application in real-world agricultural settings., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier Ltd. All rights reserved.)

Arsenic (As) is a toxic metalloid that is a significant global pollutant of the environment and a persistent bioaccumulation carcinogen. Earthworms are frequently employed as sentinel organisms to investigate the bioavailability of As in contaminated soils. However, the process of As accumulation in earthworms and the mechanism of transformation of As species in their bodies are not well understood. The accumulation of As and variation of As species in the earthworms (Eisenia fetida) exposed to sodium arsenite (0, 20, and 80 mg kg -1 As) were investigated in this study. The total As concentration of earthworms in the three treatments at various sample times was dose-dependent on soil As content. After 56 days of exposure, the high concentration treatment had the highest total As content (772 ± 21 mg kg -1 ) in earthworms, followed by the low concentration treatment (579 ± 42 mg kg -1 ) and control (31 ± 1 mg kg -1 ). During 56 days, the proportion of trivalent As in earthworms increased from 70% to more than 90%, while pentavalent As decreased by 11-18%. On day 28, the sum of the four organic As species reached a maximum (<1%). Changes in soil As species and an increase in bioavailable As cause earthworms to accumulate more As. The total As in soil after 56 days of exposure was 9.51 ± 0.50, 25.6 ± 0.60, and 82.8 ± 0.28 mg kg -1 , which was not significantly different from the total As in soil before the experiment. These findings are useful in assessing the risk of earthworm exposure to sodium arsenite in the soil., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier Ltd. All rights reserved.)

It is now well-established that arsenic exposure induces hypertension in humans. Although arsenic-induced hypertension is reported in many epidemiological studies, the underlying molecular mechanism of arsenic-induced hypertension is not fully characterized. In the human body, blood pressure is primarily regulated by a well-known physiological system known as the renin-angiotensin system (RAS). Hence, we explored the potential molecular mechanisms of arsenic-induced hypertension by investigating the regulatory roles of the RAS. Adult C57BL/6JJcl male mice were divided into four groups according to the concentration of arsenic in drinking water (0, 8, 80, and 800 ppb) provided for 8 weeks. Arsenic significantly raised blood pressure in arsenic-exposed mice compared to the control group, and significantly raised plasma MDA and Ang II and reduced Ang (1-7) levels. RT-PCR results showed that arsenic significantly downregulated ACE2 and MasR in mice aortas. In vitro studies of endothelial HUVEC cells treated with arsenic showed increased level of MDA and Ang II and lower levels of Ang (1-7), compared with the control. Arsenic significantly downregulated ACE2 and MasR expression, as well as those of Sp1 and SIRT1; transcriptional activators of ACE2, in HUVECs. Arsenic also upregulated markers of endothelial dysfunction (MCP-1, ICAM-1) and inflammatory cytokines (IL-6, TNF-α) in HUVECs. Our findings suggest that arsenic-induced hypertension is mediated, at least in part, by oxidative stress-mediated inhibition of ACE2 as well as by suppressing the vasoprotective axes of RAS, in addition to the activation of the classical axis., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier Ltd. All rights reserved.)

Melatonin (MT) and hydrogen sulphide (H 2 S) are recognised as vital biomolecules actively taking part in plant defence systems as free radical scavengers and antioxidants against a myriad of biotic and abiotic stressors. However, it has been yet unknown in plants subjected to arsenic (As) toxicity whether or not H 2 S interacts with MT to regulate endogenous antioxidant defence system. Prior to beginning As stress (As–S) treatments, MT (0.10 mM) was applied externally to plants daily for three days. AsS was then started for two weeks with As(V) (0.1 mM as Na 2 HAsO 4 ·7H 2 O). The treatment of As reduced plant biomass (24.4%) and chlorophyll a (51.7%), chlorophyll b (25.9%), while it increased subcellular As in roots and leaves, levels of glutathione (GSH), hydrogen peroxide (H 2 O 2), malondialdehyde (MDA), methylglyoxal (MG), H 2 S and phytochelatins (PCs) in pepper plants. In As-stressed pepper plants, the application of MT increased plant biomass (16.3%), chlorophyll a (52.7%), chlorophyll b (28.2%), antioxidant enzymes' activities, and H 2 S accumulation, while it lowered the concentrations of MDA and H 2 O 2. In As-treated plants, GSH and phytochelatins (PCs) were increased by MT by regulating As sequestration to make it harmless. The addition of MT increased As accumulation in the vacuoles of roots and caused the soluble fraction of As in vacuoles to become less toxic to vital organelles. MT-induced tolerance to As stress was further enhanced using NaHS, a source of H 2 S. Hypotaurine (0.1 mM HT), a H 2 S scavenger, was applied to the control and As-stressed plants together with MT and MT + NaHS to determine whether H 2 S was implicated in MT-induced increased As–S tolerance. By reducing H 2 S generation in pepper plants, HT counteracted the beneficial effects of MT, whereas the addition of NaHS to MT + HT restored the negative effects of HT, proving that H 2 S is necessary for the pepper plants As-stress tolerance caused by MT. [Display omitted] • Arsenic stress (AsS) led to a marked reduction in plant growth and oxidative stress in pepper. • MT markedly eliminated the As-induced growth inhibition and oxidative stress. • MT increased the intrinsic level of H 2 S as well as induced the antioxidant defence system. • MT promoted accumulation of soluble form of As in root and leaf vacuoles thereby reducing its toxicity. • The scavenger of H 2 S, HT, inverted the effect of MT by decreasing H 2 S content. [ABSTRACT FROM AUTHOR]

Arsenic is a ubiquitous element found in the earth crust with a varying concentration in the earth soil and water. Arsenic has always been under the scanner due to its toxicity in human beings. Contamination of arsenic in drinking water, which generally finds its source from arsenic-containing aquifers; has severely threatened billions of people all over the world. Arsenic poisoning is worse in Bangladesh where As(III) is abundant in waters of tube wells. Natural occurrence of arsenic in groundwater could result from both, oxidative and reductive dissolution. Geothermally heated water has the potential to liberate arsenic from surrounding rocks. Inorganic arsenic has been found to have more toxicity than the organic forms of arsenic. MMA and DMA are now been considered as the organic arsenic compounds having the potential to impair DNA and that is why MMA and DMA are considered as carcinogens. Endless efforts of researchers have elucidated the source, behavior of arsenic in various parts of the environment, mechanism of toxicity and various remediation processes; although, there are lots of areas still to be addressed. In this article, attempts have been made to lay bare an overview of geochemistry, toxicity and current removal techniques of arsenic together. [ABSTRACT FROM AUTHOR]

Arsenic (As) is a common environmental pollutant that seriously interferes with the normal growth of organisms. There is an urgent need to take environment-safe and efficient strategies to mitigate As toxicity. Melatonin (MT) is a pleiotropic molecule that regulates plant growth and organ development and alleviates heavy metal stresses. The experiment aims to explore the mechanism of MT in reducing arsenite toxicity by hydroponic rice seedlings. The results showed that MT application reduced the As content in rice roots and shoots by 26.4% and 37.5%, respectively, and mainly decreased As content in the soluble fractions of the rice root cell. MT application also increased the As content of chelated-soluble pectin and alkali-soluble pectin in the cell wall by 14.7% and 74.4%, respectively. It promoted the generation of the functional group of the root cell walls by the FTIR analysis, indicating that MT may promote the fixation of As on the cell wall. Meanwhile, MT contributed to scavenging excess H 2 O 2 , reducing MDA content, and maintaining normal morphology of root cells by stimulating SOD, POD and CAT activities and increasing the level of GSH. The research deepens our understanding of how MT participates in maintaining redox homeostasis in rice cells, reducing As toxicity, and decreasing As concentration in rice seedlings, thereby providing more possibilities for reducing As accumulation in rice., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022. Published by Elsevier Ltd.)

In the current study, plant growth-promoting rhizobacterium Bacillus amyloliquefaciens SN13 (SN13) was evaluated for arsenic (As) toxicity amelioration potential under arsenate (AsV) and arsenite (AsIII) stress exposed to rice (Oryza sativa var Saryu-52) plants for 15 days. The PGPR-mediated alleviation of As toxicity was demonstrated by modulated measures such as proline, total soluble sugar, malondialdehyde content, enzymatic status, relative water content, and electrolytic leakage in treated rice seedlings under arsenic-stressed conditions as compared to the respective control. SN13 inoculation not only improved the agronomic traits but also modulated the micronutrient concentrations (Fe, Mo, Zn, Cu, and Co). The desirable results were obtained due to a significant decrease in the AsIII and AsV accumulation in the shoot (47 and 10 mg kg -1 dw), and the root (62 and 26 mg kg -1 dw) in B. amyloliquefaciens inoculated seedlings as compared to their uninoculated root (98 and 43 mg kg -1 dw) and shoot (57 and 12 mg kg -1 dw), respectively. Further, metabolome (GC-MS) analysis was performed to decipher the underlying PGPR-induced mechanisms under arsenic stress. A total of 67 distinct metabolites were identified, which influence the metabolic and physiological factors to modulate the As stress. The expression analysis of metabolism- and stress-responsive genes further proclaimed the involvement of SN13 through modulating the carbohydrate metabolism in rice seedlings, to enable improved growth and As stress tolerance., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 Elsevier Ltd. All rights reserved.)

Awareness of toxicokinetics at the subcellular level is crucial to deciphering the underlying intoxication processes of metal(loid)s, although this information is often lacking. Here, the toxicokinetics of two non-essential metal(loid)s (Cd and As) and one essential metal (Zn) in both the whole body and subcellular fractions of earthworm (Eisenia fetida) were assessed. Earthworms were exposed to natural soils originating from a gradient of metal(loid) pollution for 14 days followed by a 14-day elimination phase in clean soil. Clearly distinct toxicokinetic patterns were found in the earthworms according to the metal(loid) considered. An obvious concentration-dependent increase was observed in earthworms or subcellular compartments where no equilibrium was reached (with slow or no elimination) for Cd and As throughout the experiment. As for Zn, the earthworms were able to retain a steady-state concentration of Zn in its body or each fraction without a clear intake behavior via the dynamic trade-off between uptake and elimination at different pollution levels. These differences in toxicokinetics at the subcellular level supported the observed differences in bioaccumulation patterns and were indicative of the strategy by which non-essential and essential elements are handled by earthworms. Notably, the concentration of Cd and As in subcellular compartments showed the same pattern as for Zn in the order of cellular cytosol > cellular debris > metal-rich granules, which might be associated with the binding of non-essential/essential elements with metallothionein enriched in the cytosol. Our findings enhance the understanding of the underlying mechanisms for metal(loid) accumulation kinetics in earthworms from the perspective of subcellular partitioning, and will be beneficial for accurate risk assessment of Cd, As, and Zn., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 Elsevier Ltd. All rights reserved.)

There are numerous studies showing that exposure to arsenic (As) or fluoride (F) damages the nervous system, but there is no literature investigating the effects of combined As and F exposure to induce autophagy on neurotoxicity in the offspring. In this study, we developed a rat model of As and/or F exposure through drinking water from before pregnancy to 90 days postnatal. The offspring rats were randomly divided into nine groups. Sodium arsenite (NaAsO 2 ) (0, 35, 70 mg/L) and Sodium fluoride (NaF) (0, 50, 100 mg/L) were designed according to 3 × 3 factorial design. Our results suggested that the presence of F might antagonize the excretion of total As in urine, and As-F co-exposure led to severe pathological damage in brain tissue and reduced spatial learning and memory ability. At the same time, the experiments showed that As and F increased Beclin1 expression and LC3B ratio to activate autophagy; both P62 and Lamp2 expression were increased, suggesting that autophagy lysosomal degradation was blocked; SYN and JIP1 expression were significantly decreased, disrupting synaptic structure and function. Axonal autophagosome reverse transport regulation might be affected by combined As-F exposure, exacerbating neuronal synaptic damage and inducing neurotoxicity. Further analysis showed that there was an interaction between As and F exposure-induced changes in autolysosome-related proteins in the hippocampus, which showed antagonism, and the antagonism of the high As combined exposure groups were stronger than that of the low As combined exposure groups. In conclusion, our study showed that combined As and F exposure might induce reverse transport impairment of autophagy on axons, leading to autophagy defects, which in turn led to disruption of synaptic morphology and function, induced neurotoxicity, and there was an interaction between As and F, the type of its combined effect was antagonism., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 Elsevier Ltd. All rights reserved.)

Despite the growing concerns about arsenic toxicity, information on tolerance and responsible genetic factors in wheat remains elusive. To address that, the present study aimed to screen the wheat varieties against arsenic based on growth parameters, yield, grain accumulation, and associated genes. A total of 110 wheat varieties were grown in arsenic-contaminated regions to record physio-morphological traits. The wheat 90K Infinium iSelect SNP array was used for the genome-wide association model to identify genomic regions. Wheat varieties such as Punjab-81, AARI-11, and Daman showed arsenic concentrations >45 μg/kg in similar conditions as well as the impact on grain yield, chlorophyll, Thousand Kernel Weight, and plant height. Contrastingly, varieties like Kohistan-97, As-2002, Barani-70, and Pari-73 showed grain concentrations <5 μg/kg grown under highly contaminated conditions. Three significant loci associated with arsenic accumulation in grain were identified on chromosomes 6A (qASG1-6A) and 6B (qASG3-6B and qASG4-6B). Annotation at these loci identified 39 wheat genes among which several were important for growth and tolerance against stress. The candidate gene (TraesCS6B02G429400) responsible for Glutathione-S-transferase was identified in the present study and must be investigated further using a transcriptomic approach. The present study provided background information for breeding prospects to improve wheat yield and tolerance against arsenic., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 Elsevier Ltd. All rights reserved.)

The use of macrophytes has been proposed recently as a suitable option for the phytostabilization or rhizofiltration of soils or waters contaminated by trace elements. As one of the most representative species of this type of plant, common reed (Phragmites australis (Cav.) Trin. ex Steud.) has shown tolerance to high concentrations of potentially hazardous elements, as is the case of arsenic. However, a deeper knowledge of how these plants deal with this toxicity, including their oxidative response, is needed for the optimum utilization of this species in phytoremediation procedures. In fact, little is known about how common reed plants react to As toxicity or the tolerance limits and accumulation potential of this species. In this work, common reed plants were exposed to a range of As(V) mass concentrations (0.5-10 mg L -1 ) in a hydroponic experiment, and the performance of the plants (growth, photosynthetic pigments, and oxidative stress related parameters) was evaluated and related to the major As species present in the different parts of the plants. The plants did not show any apparent symptom of toxicity and no significant effects were found for any of the different plant parameters analyzed. Arsenic was mostly accumulated as As(III) in the roots of the plants, and almost no translocation to the aerial part of the plants was observed for any of the As species analyzed. Common reed has shown a high capacity for As accumulation in its roots with no signs of toxicity, despite small nutrient imbalances. Thus, it can be considered to be a good candidate for use in the rhizofiltration and phytostabilization of As contaminated waters and soils, respectively., (Copyright © 2022 The Authors. Published by Elsevier Ltd.. All rights reserved.)

The ecological risks caused by the coexistence of pollutants such as arsenic (As) and polystyrene-nanoplastics (PSNPs) in the environment have become a non-negligible problem. However, the effects of As and PSNPs co-exposure on mammals and the underlying toxicity mechanisms have remained unclear. Therefore, the present study established mouse models of As and/or PSNPS exposure to systematically analyze the underlying role of autophagy, apoptosis and pyroptosis in hepatotoxicity induced by co-exposure of As and PSNPs. Our findings demonstrated for the first time that mice co-exposure to As and PSNPs displayed significant pathological changes in the liver, while exposure to As or PSNPs alone did not produce significant toxic effects. More importantly, As and PSNPs co-exposure activated excessive autophagy through altered expression levels of PI3K, mTOR, Beclin-1, ATG5, LC3 and P62. Meanwhile, co-treatment with As and PSNPs induced apoptosis in the liver, which was confirmed by ultrastructure observation and changes in the expression of apoptosis indicators (P53, Bax, Bcl-2, Caspase-3, Caspase-9, Cleaved-Caspase-3 and Cytc). Additionally, co-exposure of As and PSNPs induced pyroptosis in the liver through NLRP3/Caspase-1 pathway via targeting NLRP3, ASC, Pro-Caspase-1, GSDMD and Cleaved-Caspase-1 expressions. Overall, our findings provide deeper insight into the roles of apoptosis, pyroptosis and excessive autophagy in the aggravation of liver injury, which could contribute to a better understanding of the interactions between As and PSNPS exposure and the molecular mechanisms of hepatotoxicity., (Copyright © 2022 Elsevier Ltd. All rights reserved.)

Parkinson's disease (PD) is a neurodegenerative condition characterized by the dopamine (DA) neuronal loss in the substantia nigra. PD impairs motor controls symptoms such as tremor, rigidity, bradykinesia and postural imbalance gradually along with non-motor problems such as olfactory dysfunction, constipation, sleeping disorder. Though surplus of factors and mechanisms have been recognized, the precise PD etiopathogenesis is not yet implied. Reports suggest that various environmental factors play a crucial role in the causality of the PD cases. Epidemiological studies have reported that heavy metals has a role in causing defects in substantia nigra region of brain in PD. Though the reason is unknown, exposure to heavy metals is reported to be an underlying factor in PD development. Metals are classified as either essential or non-essential, and they have a role in physiological processes such protein modification, electron transport, oxygen transport, redox reactions, and cell adhesion. Excessive metal levels cause oxidative stress, protein misfolding, mitochondrial malfunction, autophagy dysregulation, and apoptosis, among other things. In this review, we check out the link between heavy metals like copper (Cu), arsenic (As), cadmium (Cd), iron (Fe), and lithium (Li) in neurodegeneration, and how it impacts the pathological conditions of PD. In conclusion, increase or decrease in heavy metals involve in regulation of neuronal functions that have an impact on neurodegeneration process. Through this review, we suggest that more research is needed in this stream to bring more novel approaches for either disease modelling or therapeutics., (Copyright © 2022 Elsevier Ltd. All rights reserved.)

To investigate prenatal exposure to arsenic and its effect on birth size, we conducted a cross-sectional study in Wujiang City, Jiangsu, China, from June 2009 to June 2010. A total of 1722 mother-infant pairs were included in the study. A questionnaire was administered to the pregnant women and umbilical cord blood(UCB) samples were collected. Arsenic concentration in UCB was detected by inductively coupled plasma emission mass spectroscopy (ICP-MS). The birth size included birth weight, birth body length and head circumference of the newborns. The effects of arsenic exposure on birth size were assessed by multiple linear regression analysis. Arsenic concentrations in UCB ranged from 0.11 to 30.36 μg/L, the median was 1.71 μg/L. In this range of exposure, arsenic concentration was significantly negatively associated with birth weight, especially among male infants. Our results showed that prenatal exposure to arsenic level was low in Wujiang City, China. However, low prenatal arsenic exposure could have negative effects on birth weight. Our research provided evidence for the adverse effects of prenatal low-level arsenic exposure on the intrauterine growth of the fetus., (Copyright © 2022. Published by Elsevier Ltd.)

During this study, the bioremediation potential of zinc-oxide nanoparticles (ZnO-NPs) and PGPR mixed biofertilizer (BF) on maize plants under induced arsenic (As) stress of 50 ppm and 100 ppm was investigated. The treated plants showed increased As resistance to mitigate the adverse effects of stress by enhancing fresh and dry biomass, relative water content, protein content, soluble sugars, proline content, enzymatic antioxidant defense mechanisms including activities of catalase (CAT), peroxidase (POD), ascorbate peroxidase (APX), superoxide dismutase (SOD), and malondialdehyde (MDA) content. In the pot experiment, the parameters studied have shown that the integrated treatments of ZnO-NPs and BF cause a notable enhancement in relative water content 43%-50% and plant biomass. Moreover, the same treatment showed a marked upregulation in enzymes activity (APX, SOD, APX, and CAT) which oxidized the cell-damaging ROS, produced in response to As stress. Likewise, the combined treatment showed a maximum reduction in MDA content 46%-57% and electrolyte leakage in As treated plants as compared to stressed plants. On the other hand, total soluble sugar 114%-170% and total protein content 117%-241% escalated. SEM analysis revealed marked damage reduction in the treated cells caused by arsenic toxicity. Thus, the use of BF comprised of rhizobacteria along with ZnO-NPs could be a very effective bio source for improving maize plant growth under As stress. In in silico study, As mediated network of proteins showed positive and negative regulation of As activity that leads to stress generation for housekeeping genome., (Copyright © 2022 Elsevier Ltd. All rights reserved.)

Pot experiments were carried out to examine the biochar application and its alleviating effect on arsenic (As) toxicity in soybean plants. The data showed that As inhibits the growth indices and it increased with enhanced As-concentration in the substrate. The growth indices declined by more than 40% and the osmolyte concentration, photosynthetic pigments and antioxidant enzymes were decreased significantly among As-stressed plants. However, biochar application effectively mitigated the inhibitory effects of As on the soybean growth and the mitigation effect of treatment is more prevalent to the plants subjected to higher As-treatment. Biochar significantly reduced the As-uptake as revealed by the translocation factor (<1), indicating more As is restrained in the roots. The reduction in the total chlorophyll and carotenoid content was found less in the As-treated soybean plants upon biochar application. Similarly, the osmolytes comprising proline, sugar and protein increased upon application of biochar. The biomarkers viz., membrane stability index (MSI), hydrogen peroxide and malondialdehyde (MDA) content significantly decreased at higher As-levels upon biochar application as was also supported by the heatmap analysis. Moreover, the antioxidative enzymes also showed a significant increase upon addition of biochar. Our data showed that biochar amendment effectively alleviates the As-stress by enhancing the sorption of As in the substrate thus, significantly declining the As concentration in plant leaves, and thus the results of the current study depicting the role of biochar as a promising, cost-effective and eco-friendly amendment to decontaminate the As-polluted soils., (Copyright © 2021 Elsevier Ltd. All rights reserved.)

Thiourea (TU) is a chemo-priming agent and non-physiological reactive oxygen species (ROS) scavenger whose application has been found to reduce As accumulation in rice grains along with improved growth and yield. The present field study explored TU-mediated mechanistic changes in silicon (Si) assimilation in root/shoot, biochemical and molecular mechanisms of arsenic (As) stress amelioration in rice cultivars. Gosai and Satabdi (IET-4786) rice cultivars were selected for field experiment at three different places; control field and two other As contaminated experimental fields (EF1 and EF2) in West Bengal, India. The average As reduction was observed to be 9.5% and 19.8% whereas the yield increment was 8.8% and 17.7% for gosai and satabdi, respectively among all the three experimental fields. The positive interrelation was also observed between improved internal ultrastructure anatomy and enhanced Si assimilation (36%-423%) upon TU application. The level of photosynthetic pigments was increased by 29.8%-99.2%. Further, activities of antioxidant enzymes were harmonically altered in TU supplemented plants. The expression of various As related transporter genes in flag leaf and developing grains (inflorescence) was changed in both the rice cultivars (gosai and satabdi). It was also presumably responsible for observed As reduction in grains. Thus, TU application was found to be an efficient and sustainable agronomic practice for amelioration of As toxicity in rice plants in As contaminated field conditions., (Copyright © 2022 Elsevier Ltd. All rights reserved.)

Exposure to arsenic (As), an environmental toxicant, causes damages to the central nervous system (CNS) structure and function. Emerging epidemiological studies support that exposure to As, especially during the critical periods of the CNS development, may act as an environmental risk factor of autism spectrum disorders (ASD), which is characterized by behavioral changes, including abnormal social behaviors, restricted interests and repetitive behaviors. However, direct evidence supporting the cause-effect relationship between As exposure and the risk of ASD is still missing. Thus, we aimed to investigate whether As exposure during pregnancy and lactation led to autism-like behaviors in offspring mice in the present study. We established a mice model of exposure to As via drinking water during pregnancy and lactation and conducted a battery of behavioral tests to evaluate social behaviors, repetitive behaviors, anxiety behaviors and learning and memory ability in offspring mice. We found that perinatal exposure to As caused autism-like behaviors in male offspring, which demonstrated by abnormal social behaviors and repetitive behaviors. Anxiety-like behaviors, and learning and memory impairments, known as concomitant behavioral phenotypes in mice with autism-like behaviors, were also observed. Decreases of synaptic density, especially in cortex, hippocampus and cerebellum, are extensively observed in both ASD patients and animal models of ASD. Thus, immunofluorescence staining and western blotting were used to observe the expression of PSD-95 and SYP, well-known markers for presynaptic and postsynaptic membranes, to assess the synaptic density in offspring cortex, hippocampus and cerebellum. We found perinatal exposure to As decreased the expression of PSD-95 and SYP in these brain regions. This indicated that perinatal exposure to As caused decreases of synaptic density, a typical autism-like cellular alteration in brains, which may contribute to autism-like behaviors in offspring., (Copyright © 2021 Elsevier Ltd. All rights reserved.)

Eco-toxicological assays with species of economic interest such as Diacronema lutheri are essential for industries that produce aquaculture feed, natural food additives and also in drug developing industries. Our study involved the exposure of a single and combined toxicity of arsenic (As V) to D. lutheri for the entire algal growth phase and highlighted that a combined exposure of As V with other essential (Copper, Cu; Nickel, Ni) and non-essential (Cadmium, Cd; Lead, Pb) trace metals reduced significantly the cell number, chlorophyll a content, and also significantly increased the de-epoxidation ratio (DR) as a stress response when compared to the single toxicity of As V. Arsenic, as one of the ubiquitous trace metal and an active industrial effluent is reported to have an increased bio-concentration factor when in mixture with other trace metals in this study. In the combined exposure, the concentration of total As bio-accumulated by D. lutheri was higher than in the single exposure. Hence, polluted areas with the prevalence of multiple contaminants along with the highly toxic trace metals like As can impose a greater risk to the exposed organisms that may get further bio-magnified in the food chain. Our study highlights the consequences and the response of D. lutheri in terms of contamination from single and multiple trace metals in order to obtain a safer biomass production for the growing need of natural derivatives., (Copyright © 2021 Elsevier Ltd. All rights reserved.)

Exposure to arsenic (As) or fluoride (F) has been shown to cause cardiovascular disease (CVDs). However, evidence about the effects of co-exposure to As and F on myocardium and their mechanisms remain scarce. Our aim was to fill the gap by establishing rat and H9c2 cell exposure models. We determined the effects of As and/or F exposure on the survival rate, apoptosis rate, morphology and ultrastructure of H9c2 cells; in addition, we tested the related genes and proteins of endoplasmic reticulum stress (ERS) and apoptosis in H9c2 cells and rat heart tissues. The results showed that As and/or F exposure induced early apoptosis of H9c2 cells and caused endoplasmic reticulum expansion. Additionally, the mRNA and protein expression levels of GRP78, PERK and CHOP in H9c2 cells were higher in the exposure groups than in the control group, and could be inhibited by 4-PBA. Furthermore, we found that As and/or F exposure increased the expression level of GRP78 in rat heart tissues, but interestingly, the expression level of CHOP protein was increased in the F and As groups, while significantly decreased in the co-exposure group. Overall, our results suggested that ERS-induced apoptosis was involved in the damage of myocardium by As and/or F exposure. In addition, factorial analysis results showed that As and F mainly play antagonistic roles in inducing myocardial injury, initiating ERS and apoptosis after exposure., (Copyright © 2021 Elsevier Ltd. All rights reserved.)

Being analogue to arsenic (As), phosphorus (P) may affect As dynamics in soil and toxicity to plants depending upon many soil and plant factors. Two sets of experiments were conducted to determine the effect of P on As fractionation in soils, its accumulation by plants and subsequent impact on growth, yield and physiological characteristics of sunflower (Helianthus annuus L.). Experimental plan comprised of two As levels (60 and 120 mg As kg -1 soil), four P (0-5-10-20 g phosphate rock kg -1 soil) and three textural types (sandy, loamy and clayey) with three replications. Among different As fractions determined, labile, calcium-bound, organic matter-bound and residual As increased while iron-bound and aluminum-bound As decreased with increasing P in all the three textural types. Labile-As percentage increased in the presence of P by 16.9-48.0% at As60 while 36.0-68.1% at As120 in sandy, 19.1-64.0% at As60 while 11.5-52.3% at As120 in loamy, and 21.8-58.2% at As60 while 22.3-70.0% at As120 in clayey soil compared to respective As treatment without P. Arsenic accumulation in plant tissues at both contamination levels declined with P addition as evidenced by lower bioconcentration factor. Phosphorus mitigated the As-induced oxidative stress expressed in term of reduced hydrogen peroxide, malondialdehyde while increased glutathione, and consequently improved the achene yield. Although, P increased As solubility in soil but restricted its translocation to plant, leading to reversal of oxidative damage, and improved sunflower growth and yield in all the three soil textural types, more profound effect at highest P level and in sandy texture., (Copyright © 2021 Elsevier Ltd. All rights reserved.)

Globally, environmental contamination by potentially noxious metalloids like arsenic is becoming a critical concern to the living organisms. Arsenic is a non-essential metalloid for plants and can be acclimatised in plants to toxic levels. Arsenic acquisition by plants poses serious health risks in human due to its entry in the food chain. High arsenic regimes disturb plant water relations, promote the generation of reactive oxygen species (ROS) and induce oxidative outburst in plants. This review evidences a conceivable tie-up among arsenic levels, speciation, its availability, uptake, acquisition, transport, phytotoxicity and arsenic detoxification in plants. The role of different antioxidant enzymes to confer plant tolerance towards the enhanced arsenic distress has also been summed up. Additionally, the mechanisms involved in the modulation of different genes coupled with arsenic tolerance have been thoroughly discussed. This review is intended to present an overview to rationalise the contemporary progressions on the recent advances in phytoremediation approaches to overcome ecosystem contamination by arsenic., (Copyright © 2021 Elsevier Ltd. All rights reserved.)

The soil protistan community makes important contributions to the ecological functions of soil. However, our knowledge of the effects of pollutants, especially plastic particles, on the soil protistan community is still very limited compared to our knowledge on other soil microbes, such as bacterial and fungi. In this study, we revealed the effects of combined and single pollution caused by arsenic (As) and microplastics/nanoplastics (MPs/NPs) on bacterial, fungal and protistan communities. Our results revealed that combined pollution through As and MPs/NPs distinctly affected the composition and structure of the soil protistan communities (P < 0.05), but in the case of bacteria, only some families were altered, and there was no impact on fungi. Changes of soil protistan communities might be mainly due to As pollution, and MPs/NPs exposure increased this detrimental effect. Further, As + MPs exposure greatly increased the abundance of soil protistan parasites, and As + NPs exposure caused an evident decrease in the abundance of soil protistan consumers (P < 0.05). These findings indicate that combined pollution by As and MPs/NPs can affect the ecological functions of soil by altering soil protistan communities. These results will help enhance our understanding of the impact of plastic particles on soil ecosystems., (Copyright © 2021 Elsevier Ltd. All rights reserved.)

Despite the urge need to address the possible impact of plastic debris, up to now, little is known about the translocation of nanoplastics through the trophic web. Plus, due to their surface reactivity, nanoplastics could sorb and thus increase metals bioavailability to aquatic filter-feeding organisms (e.g., bivalves). In this study, we investigated the dietary exposure route on the oyster Crassostrea virginica through microalgae themselves exposed to three nanoplastic dispersions (PSL, PSC and NPG) at reportedly environmental concentrations combined or not with arsenic. Interactive effects of nanoplastics on arsenic bioaccumulation were studied, along with the expression of key genes in gills and visceral mass. The investigated gene functions were endocytosis (cltc), oxidative stress (gapdh, sod3, cat), mitochondrial metabolism (12S), cell cycle regulation (gadd45, p53), apoptosis (bax, bcl-2), detoxification (cyp1a, mdr, mt), and energy storage (vit). Results showcased that nanoplastic treatments combined with arsenic triggered synergetic effects on gene expressions. Relative mRNA level of 12S significantly increased at 10 and 100 μg L -1 for NPG combined with arsenic and for PSC combined with arsenic. Relative mRNA level of bax increased for PSL combined with arsenic and for PSC combined with arsenic at 10 and 100 μg L -1 respectively. We also observed that relative arsenic bioaccumulation was significantly higher in Crassostrea virginica gills compared to Isognomon alatus'. These results are the first comparative molecular effects of nanoplastics alone and combined with arsenic investigated in farmed C. virginica oysters. Together with I. alatus results we thus shed light on species different sensitivity., (Copyright © 2021 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Chronic arsenic toxicity has become a global concern due to its adverse pathophysiological outcome and carcinogenic potential. It is already established that arsenic induced reactive oxygen species alters mitochondrial functionality. Major regulatory genes for mitochondrial biogenesis, i.e., PGC1α, Tfam, NRF1 and NRF2 are located in the nucleus. As a result, mitochondria-nucleus crosstalk is crucial for proper mitochondrial function. This previous hypothesis led us to investigateinvolvement of epigenetic alteration behindenhanced mitochondrial biogenesis in chronic arsenic exposure. An extensive case-control study was conducted with 390 study participants (unexposed, exposed without skin lesion, exposed with skin lesion and exposed skin tumour) from highly arsenic exposed areas ofWest Bengal, India. Methylation specific PCRrevealed significant promoter hypomethylation oftwo key biogenesis regulatory genes, PGC1α and Tfam in arsenic exposed individuals and also in skin tumour tissues. Linear regression analysis indicated significant negative correlation between urinary arsenic concentration and promoter methylation status. Increased expression of biogenesis regulatory genes wasobtained by quantitative real-time PCR analysis. Moreover, altered mitochondrial fusion-fission regulatory gene expression was also observed in skin tumour tissues. miR663, having tumour suppressor gene like function was known to be epigenetically regulated through mitochondrial retrograde signal. Promoter hypermethylation with significantly decreased expression of miR663 was found in skin cancer tissues compared to non-cancerous control tissue. In conclusion, results indicated crucial role of epigenetic alteration in arsenic induced mitochondrial biogenesis and arsenical skin carcinogenesis for the first time. However, further mechanistic studies are necessary for detailed understanding of mitochondria-nucleus crosstalk in arsenic perturbation. Image 1 • Mitochondria-nucleus crosstalk plays critical role in arsenic induced skin cancer. • Arsenic induces epigenetic alteration in mitochondrial biogenesis regulatory genes. • Enhanced mitochondrial biogenesis and high mtDNA copy number in arsenical skin cancer. • MiR663 might influence arsenic induced skin carcinogenesis by mitochondrial alteration. • Chronic arsenic toxicity results in altered mitochondrial fusion-fission dynamics. [ABSTRACT FROM AUTHOR]

Heavy metals pose a serious threat if they go beyond permissible limits in our bodies. Much heavy metal's viz. Lead, Chromium, Arsenic, Mercury, Nickel, and Cadmium pose a serious threat when they go beyond permissible limits and cause hepatotoxicity. They cause the generation of ROS which in turn causes numerous injuries and undesirable changes in the liver. Epidemiological studies have shown an increase in the levels of such heavy metals in the environment posing a serious threat to human health. Epigenetic alterations have been seen in the event of exposure to such heavy metals. Apoptosis, caspase activation as well as ultrastructural changes in the hepatocytes have also been seen due to heavy metals. Inflammation involving TNF-alpha, pro-inflammatory cytokines, MAPK, ERK pathways have been seen in the event of heavy metal hepatotoxicity. All these have shown that these heavy metals pose a serious threat to human health in particular and the environment as a whole., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2021 Elsevier Ltd. All rights reserved.)

Arsenic and fluoride are two naturally occurring toxicants to which various organisms including a major part of the human populations are co-exposed to. However, interactions between them inside body are quite complicated and needs proper evaluation. Inconclusive reports regarding their combined effects on brain prompted us to conduct this study where we investigated their individual as well as combined effects on female zebrafish brain at environmentally relevant concentrations (50 μgL -1 arsenic trioxide and 15 mgL - 1 sodium fluoride) after different time intervals (15, 30 and 60 days). Persistent near-basal level of GSH, least increased MDA content and catalase activity portrayed arsenic and fluoride co-exposure as less toxic which was corroborated with far less damage caused in the histoarchitecture of optic tectum region in midbrain. Stress-responsive genes viz., Nrf2 and Hsp70 were overexpressed after individual as well as combined exposures, indicating a common cellular response to combat the formed oxidative stresses. Biphasic response of AChE upon individual exposure confirmed their neurotoxic effects too. Expression profile of p53 (unaltered), Bax (lower or near-basal) and Bcl2 (comparatively higher), along with absence of DNA fragmentation indicated no induction of apoptosis in the co-exposed group. Tissue accumulation of arsenic and fluoride was significantly less in the brain of co-exposed zebrafish when compared to their individual exposures. This preliminary study indicates an antagonistic effect of these two toxicants in zebrafish brain and needs further studies involving oxidative stress independent markers to understand the detailed molecular mechanism., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financialinterestsor personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020 Elsevier Ltd. All rights reserved.)

Arsenic is a well-established human carcinogen and is considered a health risk worldwide, especially where groundwater is consumed as drinking water. In 2018, bladder and kidney cancers were the 14th and 17th leading causes of global cancer mortality, respectively. Our aim was to investigate the association between arsenic exposure, DNA damage, and the incidence of bladder and kidney cancers. A total of 788 participants aged ≥40 years were enrolled in a prospective cohort study in Taiwan between 1991 and 1994, with follow-up between 2011 and 2014. Well-water and first-morning spot urine samples were collected between 1991 and 1994 to estimate arsenic exposure, and the baseline urinary levels of 8-Oxo-2'-deoxyguanosine (8-OHdG) and N7-methylguanine (N7-MeG) were quantified to assess DNA lesions. The Cox proportional hazard model was used to estimate the effects of arsenic exposure and DNA adduct levels on the risk of bladder or kidney cancer. Urinary arsenic species were associated with significantly increased 8-OHdG and N7-MeG after adjusting for age, sex, and cigarette smoking. Only non-statistically significant mediation effects of 8-OHdG were observed. In a fully adjusted Cox model, participants with arsenic exposure and urinary 8-OHdG levels higher than the median had a higher risk of bladder cancer (HR = 4.60, confidence interval: 1.43-14.85). Overall, the combined effects of high cumulative arsenic exposure from artesian well-water and advanced DNA damage predicted the risk of bladder cancer., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020 Elsevier Ltd. All rights reserved.)

Inorganic arsenic, a well-known human carcinogen, poses a major threat to global health. Given the immunosuppressive potentials of inorganic arsenic as well as limited understanding of this metalloid on antigen-presenting dendritic cells (DCs), we systematically screened the immune targets in response to arsenic treatment, as well as its possible molecular mechanism in cultured murine DCs. Our results denoted that arsenite (As) significantly induced immune tolerance by down-regulating the expression of phenotypic molecules, pro-inflammatory factors and T-lymphocyte helper (Th)1/Th17-inducible cytokines in lipopolysaccharides (LPS)-stimulated myeloid-derived dendritic cells (BMDCs). Inconsistent with dampened phosphorylation of immune-related proteins (nuclear factor kappa-B) NF-κB, p38 and JNK, the metalloid drastically induced the expression of Heme oxygenase-1 (HO-1) protein, which enlightened us to continuously explore the possible roles of HO-1 pathway in As-induced immune tolerance in BMDCs. In this respect, immunosuppressive properties of HO-1 pathway in BMDCs were firstly confirmed through pharmacological overexpression of HO-1 by both CoPP and CORM-2. By contrast, limited HO-1 expression by HO-1 inhibitor ZnPP specifically alleviated As-mediated down-regulation of CD80, chemokine factor C-C chemokine receptor 7 (CCR7), tumor necrosis factor (TNF) -α, Interleukin (IL)-23 and IL-6, which reminds us the peculiarity of HO-1 in As-induced immune tolerance in murine DCs. Based on these experimental findings, we postulated the immunosuppressive property of inorganic arsenic might be mediated partially by HO-1 in DCs, thus contributing to the interactions of DCs-polarized differentiation of T-lymphocyte subtype as well as the development of infections and malignant diseases., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020 Elsevier Ltd. All rights reserved.)