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Chemical-induced neurotoxicity is increasingly recognized to accelerate the development of neurodegenerative disorders (NDs), which pose an increasing health burden to society. Attempts are being made to develop drugs that can cross the blood-brain barrier and have minimal or no side effects. Nobiletin (NOB), a polymethoxylated flavonoid with anti-oxidative and antiinflammatory effects, has been demonstrated to be a promising compound to treat a variety of NDs. Here, we investigated the potential role of NOB in sodium arsenate (NA)-induced deregulated miRNAs and target proteins in human neural progenitor cells (hNPCs). The proteomics and microRNA (miRNA) profiling was done for different groups, namely, unexposed control, NA-exposed, NA + NOB, and NOB groups. Following the correlation analysis between deregulated miRNAs and target proteins, RTPCR analysis was used to validate the selected genes. The proteomic analysis showed that significantly deregulated proteins were associated with neurodegeneration pathways, response to oxidative stress, RNA processing, DNA repair, and apoptotic process following exposure to NA. The OpenArray analysis confirmed that NA exposure significantly alteredmiRNAs that regulate P53 signaling, Wnt signaling, cell death, and cell cycle pathways. The RT-PCR validation studies concur with proteomic data as marker genes associated with autophagy and apoptosis (HO-1, SQSTM1, LC-3, Cas3, Apaf1, HSP70, and SNCA1) were altered following NA exposure. It was observed that the treatment of NOB significantly restored the deregulated miRNAs and proteins to their basal levels. Hence, it may be considered one of its neuroprotective mechanisms. Together, the findings are promising to demonstrate the potential applicability of NOB as a neuroprotectant against chemical-induced neurotoxicity. [ABSTRACT FROM AUTHOR]

Chemical-induced neurotoxicity is increasingly recognized to accelerate the development of neurodegenerative disorders (NDs), which pose an increasing health burden to society. Attempts are being made to develop drugs that can cross the blood–brain barrier and have minimal or no side effects. Nobiletin (NOB), a polymethoxylated flavonoid with anti-oxidative and anti-inflammatory effects, has been demonstrated to be a promising compound to treat a variety of NDs. Here, we investigated the potential role of NOB in sodium arsenate (NA)-induced deregulated miRNAs and target proteins in human neural progenitor cells (hNPCs). The proteomics and microRNA (miRNA) profiling was done for different groups, namely, unexposed control, NA-exposed, NA + NOB, and NOB groups. Following the correlation analysis between deregulated miRNAs and target proteins, RT-PCR analysis was used to validate the selected genes. The proteomic analysis showed that significantly deregulated proteins were associated with neurodegeneration pathways, response to oxidative stress, RNA processing, DNA repair, and apoptotic process following exposure to NA. The OpenArray analysis confirmed that NA exposure significantly altered miRNAs that regulate P53 signaling, Wnt signaling, cell death, and cell cycle pathways. The RT-PCR validation studies concur with proteomic data as marker genes associated with autophagy and apoptosis (HO-1, SQSTM1, LC-3, Cas3, Apaf1, HSP70, and SNCA1) were altered following NA exposure. It was observed that the treatment of NOB significantly restored the deregulated miRNAs and proteins to their basal levels. Hence, it may be considered one of its neuroprotective mechanisms. Together, the findings are promising to demonstrate the potential applicability of NOB as a neuroprotectant against chemical-induced neurotoxicity.

Biochemical and/or molecular mechanisms of arsenic or fluoride toxicity in experimental animals have been widely investigated in the recent past. However, their combined effects on target cells/organelle are poorly understood. The present study was executed to delineate their combined effects on mitochondrial function in the liver of rat. Female Wistar rats (140 ± 20 g) were force fed individually or in combination with sodium arsenate (4 mg/kg body weight) and sodium fluoride (4 mg/kg body weight) for 90 days. Thereafter, established markers of mitochondrial function viz. mitochondrial lipid peroxidation, oxidative phosphorylation, ATPase, succinic dehydrogenase, and caspase-3 activity were determined. Cytochrome C release and oxidative DNA damage were also estimated in the liver of respective groups of rats. The study showed significant differences in these results amongst the three groups. Observations on parameters viz. LPO, cytochrome-C, caspase-3, and 8-OHdG suggested an antagonistic relationship between these two elements. Results on ATPase, SDH, and ADP:O ratio indicated synergism. It is concluded that AsIII + F in combination may express differential effects on signalling pathways and proapoptotic/antiapoptotic proteins/genes that contribute to liver cell death. Interaction of As and F with mitochondria [ABSTRACT FROM AUTHOR]

Background: Sodium arsenate (Na 3As0 4, Sodium As) is an important toxic substance that leads to nephrotoxicity. Due to having bioactive molecules, such as polyphenols and tyrosol, olive oil plays a significant role in scavenging free radicals. This study aimed to investigate the effects of olive oil and tyrosol on As-induced nephrotoxicity. Methods: In our study, 42 adult male BALB/c mice were randomly divided into six groups: control (normal saline), olive oil (0.4 ml/d, gavage), tyrosol (5 mg/kg/d), Sodium As (15 mg/kg), olive oil + Sodium As, and tyrosol + Sodium As (olive oil and tyrosol received one hour before Sodium As). Drugs were administreted once daily for 30 consecutive days. On the 31st day of the study, oxidative stress parameters in kidney tissue, FRAP in plasma, renal function parameters in serum, and histopathological assays were performed. Results: Sodium As-induced renal damage as characterized by a significant increase of creatinine and BUN (P < 0.001) and histopathological changes. Also, Sodium As markedly altered oxidative stress biomarkers such as a significant increase in MDA (P < 0.001) and significantly decreased in FRAP and GSH (P < 0.01). Olive oil and tyrosol administration significantly improved the renal antioxidant defense system and decreased MDA concentration, markedly preserving the tissue structure and functional markers of kidney. However, these effects were more effective for tyrosol than olive oil. Conclusions: Our results suggest that olive oil and tyrosol can be used as a protective agent in preventing Sodium As-induced nephrotoxicity due to antioxidant property. [ABSTRACT FROM AUTHOR]

• The inorganic arsenite and arsenate found in water as the most prevalent forms. • Excessive exposure to inorganic arsenate in drinking water causes a slew of health issues in human. • Hepatocytes are exposed to xenobiotics; they undergo morphological and structural damage. • Centella asiatica has the potential to reduce the cytotoxicity triggered by sodium arsenate in zebrafish. Arsenic contamination in drinking water is a major public health concern. It is classified as an environmental pollutant that necessitates immediate corrective action. Long-term arsenic exposure may cause hepatotoxicity. The current research focuses on the effectiveness of a methanolic extract of Centella asiatica against sodium arsenate-induced hepatotoxicity in Danio rerio (Zebrafish). Phytochemicals and bioactive compounds in C.asiatica extract were studied using standard procedure and GC-MS analysis. The extract was also assessed for antioxidant and antibacterial properties. The significant scavenging activity of oxygen-free radicals as well as the IC50 values was observed. Furthermore, the ability of C.asiatica (500 mg/g) leaf extract to alleviate hepatotoxicity in Zebrafish pretreated and post-treated with sodium arsenate (100g/l) was observed. In this work, phytochemical examination of C.asiatica leaf extract revealed the presence of bioactive substances such as alkaloids, flavonoids, terpenoids, glycosides, phenolics, proteins, and carbohydrates, which was validated by GC MS analysis of different percentage areas. Importantly, the methanolic extract of C.asiatica demonstrated strong antimicrobial and antioxidant activities. The plant extract, in particular, demonstrated its efficiency by alleviating the effects of arsenate in the liver of zebrafish (both pre-and post-treatment), as demonstrated by histological analysis. The results of histopathological research revealed that methanolic extract of C.asiatica had a considerable lowering effect on sodium arsenate-induced hepatocyte damage in zebrafish. As a result, the inhibitory action of Centella asiatica methanolic extract may be investigated to create effective candidates to fight arsenate toxicity. [ABSTRACT FROM AUTHOR]

Alkaline leaching is an effective method for dealing with arsenic-containing resources. Arsenic is dissolved in an alkaline solution in the form of arsenate, but the lack of relevant basic data has caused difficulties in the theoretical analysis during production and research. The dissolution behavior of arsenic in the solution was systematically studied in this paper. The solubility behavior of the self-made sodium arsenate in water and NaOH solution were measured. The research on sodium arsenate solution was carried out to obtain the quasi-solubility product using the Pitzer model, and the effect of temperature and NaOH concentration on the solubility and quasi-solubility product of sodium arsenate was clarified.

Sodium arsenate crystals are a hazardous waste produced from the utilization of arsenic–alkali residue in antimony metallurgy that pose a serious threat to the environment. In this article, to eradicate the damage caused by sodium arsenate and enhance the sustainable development of nonferrous metallurgy, a novel process was proposed to immobilize arsenic as flaky scorodite using Fe(OH) 3 as an iron source. Various methods, such as X-ray diffraction (XRD), scanning electron microscopy (SEM), and inductively coupled plasma atomic emission spectrometry (ICP AES), were applied to characterize these synthesized products. The whole process is divided into three parts. In the thermodynamic analysis, the stable area of scorodite in the Pourbaix diagram significantly expands at high ionic activity and temperature, which favors the decrease in △ r G for scorodite synthesis, and Fe–As coprecipitation is feasible in solution at 0.18 ≤pH≤ 5.30. In the scorodite synthesis, 99.88% of the arsenic was converted to a flaky scorodite with a size of 2–5 µm by optimizing the parameters. In the removal of arsenic, residual arsenic and iron were completely coprecipitated into an iron salt by dropping NaOH solution to a final pH of 5.0. The final products include scorodite and sodium sulfate in this process. Overall, this new approach successfully eliminates the potential arsenic pollution from the utilization of arsenic–alkali residue in antimony metallurgy and can potentially be applied to dispose of other high arsenic-bearing wastes. [ABSTRACT FROM AUTHOR]

The introduction of arsenic, a hazardous metalloid, into the soil system due to heavy industrialization has negatively affected agricultural productivity, resulting in limited crop yields. A recent breakthrough in stress-responsive hormones, specifically brassinosteroids, has extensively covered the role of antioxidant enzyme defense systems in heavy metal stress mitigation. Considering the antioxidant properties and metal complex formation abilities of polyphenols, our study focuses on examining their role in arsenate toxicity amelioration by 24-epibrassinolide. We demonstrate enhanced growth parameters of sodium arsenate-stressed seedlings upon application of 24-epibrassinolide, with increased root and shoot polyphenol levels analyzed by high-performance liquid chromatography. Specifically, the concentration of catechin, sinapic acid, 4-hydroxy benzoic acid, protocatechuic acid, 4-coumaric acid, and myricetin were elevated, indicating induction of phenylpropanoid signaling pathway. Further, we also report a decrease in the generation of superoxide anions and hydrogen peroxide validated the antioxidant effects of these metabolites through the nitrobluetetrazolium and diaminobenzidine staining method. In addition, evaluation of transcript level of genes encoding for specific enzymes of the phenylpropanoid pathway in shoot and root showed a significant upregulation in mRNA expression of phenylalanine ammonia-lyase-1, cinnamate-4-hydroxylase, and caffeic acid o-methyltransferase-1 upon exogenous application of 24-epibrassinolide in arsenate stressed Oryza sativa. • 24-Epibrassinolide alleviates sodium arsenate stress in IR-20 seedlings by elevating polyphenol levels. • Exogenous 24-epibrassinolide upregulates the key enzymes of phenyl propanoid pathway in shoot. • 15 types of polyphenols were detected in Oryza sativa seedlings. • Accumulation of catechin, sinapic acid, 4-coumaric acid, myricetin, and resveratrol were high. [ABSTRACT FROM AUTHOR]

Background: In new age, Arsenic is a major environmental pollutant and exposure occurs through agricultural, environmental, medicinal and occupational sources. The toxicity of sodium arsenate has been shown in catfish, Clarias batrachus and the histology report suggested that the sodium arsenate may adversely effect on the catfish, Clarias batrachus. Methods: The histological analysis carried out during the period of 2018-19 for sodium arsenate with Clarias batrachus as test animal for 96 hour as per ideal method and determine the lethal concentration (LC50). The liver and kidney tissues were collected from the fishes exposed to sodium arsenate and standard histology procedure were followed to investigate the histological alterations. Result: Exposure of sodium arsenate causes severe histological changes in liver like nucleus blabbing, infiltration, necrosis of hepatocytes, disruption of normal architecture, shrunkeri hepatocytes, lytic hepatocytes etc. In kidney sodium arsenate exposure causes hemorrhage, inflammation and tubular atrophy in renal tubules, disruption of tubular linings, dense chronic inflammation, hemorrhage and vacoulation in Bowman's capsule etc. The present investigation suggests that the inorganic forms of arsenic showing the highest toxicity level. [ABSTRACT FROM AUTHOR]

Background: The toxic effect of sodium arsenate on nervous system has been shown; but the protective effects of several compounds against sodium arsenate are not clear. This study aimed to investigate the protective effects of nicotine and bucladesine, two positive modulators of neuronal function, on sodium arsenate toxicity against avoidance memory impairment. Methods: Male mice (N=154) were assigned to 22 groups (12 experimental and 10 control) of seven animals each and were treated as follows: sodium arsenate (2.5, 5, or 10 mg/kg) for 28 days, nicotine (1 mg/kg) for either 1, 2, or 4 days, bucladesine (600 nM/mouse) for either 1, 2, or 4 days, and nicotine (1 mg/kg)+bucladesine (600 nM/mouse)+sodium arsenate (2.5 mg/kg). The last group was treated with 2.5 mg/kg sodium arsenate first, and then received the combination of nicotine and bucladesine for 1, 2, or 4-days. The corresponding control groups did not receive any drug but either saline, deionized water, or combination of deionized water and DMSO, but went through the same procedure as other animals. All mice were trained 24 h in the step-through passive avoidance task. The avoidance memory retention was assessed at 24, 48, 96, and 168 h after the training period by measuring the time they stayed in a dark chamber. Results: All sodium arsenate doses significantly reduced the time stayed in the dark chamber regardless of the treatment duration (24, 48, 96 & 168 h) after training. Both nicotine and bucladesine, whether used singly or combined for 1, 2, and 4 days significantly enhanced the time latency compared to the controls at all of the experimental timepoints following the training. Conclusion: Nicotine and bucladesine showed synergistic effects and reversed the sodium arsenate-induced avoidance memory deficits in mice.

Environmental exposure to arsenic has been profoundly associated with chronic systemic disorders, such as neurodegeneration, in both experimental models and clinical studies. The neuronal cells of the brain and the nervous system have a limited regeneration capacity, thus making them more vulnerable to exposure to xenobiotics, leading to long-lasting disabilities. The functional and anatomical complexity of these cells hinders the complete understanding of the mechanisms of neurodegeneration and neuroprotection. The present investigations aimed to evaluate the neuroprotective efficacy of a herbal formulation of Nobiletin (NOB) against the toxic insult induced by sodium arsenate (NA) in human neural progenitor cells (hNPCs) derived from human induced pluripotent stem cells (hiPSCs). Prior to the neuroprotective experiments, biologically safe doses of both NOB and NA were ascertained using standard endpoints of cytotoxicity. Thereafter, the hNPCs were exposed to either NOB (50 μM) or NA (50 μM) and co-exposed to biologically safe concentrations of NA (50 μM) with NOB (50 μM) for a period of up to 48 h. NOB treatment restored the morphological damage (neurite damage), the levels of stress granule G3BP1 (Ras-GTPase-activating protein (SH3 domain)-binding protein) and TIA1 (T cell-restricted intracellular antigen), and the expression of neuronal markers (Tuj1, Nestin, MAP2, and PAX6) when compared to NA-exposed cells. A substantial restoration of reactive oxygen species and mitochondrial membrane potential was also witnessed in the co-exposure group (NA + NOB) in comparison to the NA-exposed group. The findings suggest that NOB possesses a significant restorative/protective potential against the NA challenge in hNPCs under experimental conditions and imply that nobiletin may impart a potential therapeutic impact if studied adequately using in vivo studies. [ABSTRACT FROM AUTHOR]

The present study aimed to assess the combined effects of arsenic (As) and fluoride (F) on liver and kidney of rat after exposure to three different time periods i.e. 30, 60, and 90 days. For this, three months old female Wistar rats were administered through gavage sodium arsenate (4 mg/kg b.w.), sodium fluoride (4 mg/kg b.w.), and sodium arsenate and sodium fluoride (4 mg/kg b.w. each) together for three-time intervals i.e. 30, 60, and 90 days. Liver function in these rats was assessed through serum enzymes and bilirubin concentration. Kidney function was estimated through creatinine and uric acid determination in urine. Findings revealed, duration of exposure to As, F, and As+F influences the hepatic and renal toxic manifestations of these elements. Bioaccumulation of As and induction of metallochaprones seem to contribute to variations in their toxicity. Whereas, some results show antagonistic relationship between As and F, others exhibit synergism between the two. Majority of present observations favour a synergistic relationship between them. However, duration of exposure and bioconcentration appear to be important variables in their combined toxicity. [ABSTRACT FROM AUTHOR]

The aim of the current study is to explain the effect of leek extract against harmful effect induced by Arsenic. Sixty adult male rats were divided into 6 groups G1 control, G2 received orally daily sodium arsenate (40 ppm) by drinking water for six weeks then left another six weeks for recovery, G3 received orally daily sodium arsenate (40 ppm) by drinking water for six weeks then intubated orally with Leek in dose (200 mg/kg B.W) for six weeks, G4 received orally daily sodium arsenate (40 ppm) by drinking water for six weeks then intubated orally with Leek in dose (100 mg/kg B.W) for six weeks, G5 received Leek in dose (200 mg/kg B.W) for six weeks then left another six weeks for recovery, G6 received Leek in dose (100 mg/kg B.W) for six weeks then left another six weeks for recovery. The experiment continue for twelve weeks. The blood samples collection by heart puncture serum separated for biochemical analysis that include Urea, Creatinine and Uric acid and samples of brain for histopathological study. The biochemical study explained that there was significant increase (p<0.05) in urea in G2,G3,G4 as compared with control group (G1) after 6 weeks, after 12 weeks there was significant increase (p<0.05) in G2,G3,G4 as compared with control group (G1). There was significant decreased in urea in G3,G4,G6 between 6weeks and 12 weeks, after 12 weeks there was significant increase (p<0.05) in G2 as compared with control group (G1). There was significant increase in Creatinine in G2, G5 between 6 weeks and 12 weeks. There was significant increase (p<0.05) in Uric acid in G2, G3, G4 as compared with control group (G1) after 6 weeks, after 12 weeks there was significant increase (p<0.05) in G2, G3, G4, G5, G6 as compared with control group (G1). There was significant decreased in Uric acid in G3 between 6weeks and 12 weeks. Histopathological result explained that there was destruction of cerebral tissue, which characterized by cavitation with various size cavities within cerebral cortex. in the groups that received Leek in dose (100, 200 mg/kg B.W) for six weeks there was the sections of the cerebrum and cerebellum have showed normal appearance and were similar to the control group. After 12 weeks there was in G2 the sections of cerebellum have revealed marked degeneration of granular layer cells and purkinje layer cells. In G3 there was the sections of both cerebellum and cerebrum were similar those in control group, in G4 there was the sections of the cerebral internal pyramidal layer have showed moderate vacular changes of astrocytes with mild tissue depletion, while the section of cerebellum have showed normal appearance. In G5, G6 there was the section of cerebrum and cerebellum of both groups were similar those of control group. [ABSTRACT FROM AUTHOR]

The aim of this study is to explain Protective effect of sesame oil (5 ml/kg B.W and2.5 ml/kg B.W) in female rats that received sodium arsenate (As+5) (40 ppm). The current two-phase study was conducted (6 and 12 weeks) and 60 female rats were used for the current studyafter dividing them evenly into six groups. The groups that were exposed to arsenic showed an increase in white blood cells, while no significant difference appeared at G5 and G6 after 6 weeks as compared with control. Also, no significant difference appeared in all groups after 12 weeks, while a significant decrease appeared in G2, G3, G4 and it did not appear any significant difference in G5, G6 when comparing the two periods. While it was noticed that there was a decrease in red blood cells and hemoglobin in the groups that were exposed to arsenic (G2, G3, G4) compared to the control after 6 weeks, while the groups that received sesame oil maintained their normal values close to the control during periods 6 and 12 weeks. It was also observed that the PLT values maintained their values within the normal values compared to control in groups (G2, G3, G4, and G6) after 6 weeks. While there was a significant decrease in PLT values at (G2, G3, G4, G6) after 12 weeks. [ABSTRACT FROM AUTHOR]

Antimicrobial resistance (AMR) is a leading cause of treatment failure for many infectious diseases worldwide. Improper overdosing and the misuse of antibiotics contributes significantly to the emergence of drug-resistant bacteria. The co-contamination of heavy metals and antibiotic compounds existing in the environment might also be involved in the spread of AMR. The current study was designed to test the efficacy of heavy metals (arsenic) induced AMR patterns in clinically isolated extended-spectrum β-lactamase (ESBL) producing bacteria. A total of 300 clinically isolated ESBL-producing bacteria were collected from a tertiary care hospital in Lahore, Pakistan, with the demographic characteristics of patients. After the collection of bacterial isolates, these were reinoculated on agar media for reidentification purposes. Direct antimicrobial sensitivity testing (AST) for bacterial isolates by disk diffusion methods was used to determine the AST patterns with and without heavy metal. The heavy metal was concentrated in dilutions of 1.25 g/mL. The collected bacterial isolates were isolated from wounds (n = 63, 21%), urine (n = 112, 37.3%), blood (n = 43, 14.3%), pus (n = 49, 16.3%), and aspirate (n = 33, 11%) samples. From the total 300 bacterial isolates, n = 172 were Escherichia coli (57.3%), 57 were Klebsiella spp. (19%), 32 were Pseudomonas aeruginosa (10.6%), 21 were Proteus mirabilis (7%) and 18 were Enterobacter spp. (6%). Most of the antibiotic drugs were found resistant to tested bacteria. Colistin and Polymyxin-B showed the highest sensitivity against all tested bacteria, but when tested with heavy metals, these antibiotics were also found to be significantly resistant. We found that heavy metals induced the resistance capability in bacterial isolates, which leads to higher AMR patterns as compared to without heavy metal tested isolates. The results of the current study explored the heavy metal as an inducer of AMR and may contribute to the formation and spread of AMR in settings that are contaminated with heavy metals.

Arsenic, an omnipresent environmental contaminant, is regarded as a potent hepatotoxin. Nigella sativa oil (NSO) consumption has been shown to improve hepatic functions in various in vivo models of acute hepatic injury. The present study evaluates the protective efficacy of NSO against sodium arsenate (As)–induced deleterious alterations in the liver. Male Wistar rats were divided into four groups, namely, control, As, NSO, and AsNSO. After pre-treating rats in AsNSO and NSO groups with NSO (2 mL/kg bwt, orally) for 14 days, NSO treatment was further extended for 30 days, with and without As treatment (5 mg/kg bwt, orally), respectively. As induced an upsurge in serum ALT and AST activities indicating liver injury, as also confirmed by the histopathological findings. As caused significant alterations in the activities of membrane marker enzymes and carbohydrate metabolic enzymes, and in the vital components of antioxidant defense system. Marked DNA damage and hepatic arsenic accumulation were also observed in As-treated rats. Oral NSO administration ameliorated these deleterious alterations and improved overall hepatic antioxidant and metabolic status in As-treated rats. Prevention of oxidative damage could be the underlying mechanism of NSO-mediated protective effects. The results suggest that NSO could be a useful dietary supplement in the management of arsenic hepatotoxicity. [ABSTRACT FROM AUTHOR]

Background: The toxic effect of sodium arsenate on nervous system has been shown; but the protective effects of several compounds against sodium arsenate are not clear. This study aimed to investigate the protective effects of nicotine and bucladesine, two positive modulators of neuronal function, on sodium arsenate toxicity against avoidance memory impairment. Methods: Male mice (N=154) were assigned to 22 groups (12 experimental and 10 control) of seven animals each and were treated as follows: sodium arsenate (2.5, 5, or 10 mg/kg) for 28 days, nicotine (1 mg/kg) for either 1, 2, or 4 days, bucladesine (600 nM/mouse) for either 1, 2, or 4 days, and nicotine (1 mg/kg)+bucladesine (600 nM/mouse)+sodium arsenate (2.5 mg/kg). The last group was treated with 2.5 mg/kg sodium arsenate first, and then received the combination of nicotine and bucladesine for 1, 2, or 4-days. The corresponding control groups did not receive any drug but either saline, deionized water, or combination of deionized water and DMSO, but went through the same procedure as other animals. All mice were trained 24 h in the step-through passive avoidance task. The avoidance memory retention was assessed at 24, 48, 96, and 168 h after the training period by measuring the time they stayed in a dark chamber. Results: All sodium arsenate doses significantly reduced the time stayed in the dark chamber regardless of the treatment duration (24, 48, 96 & 168 h) after training. Both nicotine and bucladesine, whether used singly or combined for 1, 2, and 4 days significantly enhanced the time latency compared to the controls at all of the experimental timepoints following the training. Conclusion: Nicotine and bucladesine showed synergistic effects and reversed the sodium arsenate-induced avoidance memory deficits in mice. [ABSTRACT FROM AUTHOR]

In this study we evaluated the possible teratogenic effects of arsenic (As) in the same concentrations recorded in water Zimapan, Hidalgo, using specimens of Rattus norvegicus Wistar strain, pregnant. Were subjected to varying concentrations of sodium arsenate (1887.9 mg/L, 943.9 mg/L and 0.5 mg/L), concentration, 0.5 mg/L corresponds to the registered Zimapan water, Hidalgo and chromium trioxide (166.0 mg/L) used as positive control and 5% sucrose as a negative control. The specimens were exposed from day 7 through 15 of gestation, and were sacrificed on day 19 of gestation by inhalation of chloroform. We analyzed reproductive harm the mother, as well as alterations and lack of ossification of the bone tissue of the fetus. The highest dose tested (1887.9 mg/L) produced more reproductive harm in mother resorptions caused by preventing the continuation of embryonic development. Concentrations of 0.5 mg/L to 943.9 mg/L, resulted in lack of ossification ribs, sternebrae, metacarpals, phalanges previous metatarsals and phalanges posterior sacral vertebrae.

Densities of the sodium arsenate aqueous solution with the molality varied from (0.04165 to 0.37306) mol · kg−1 were determined experimentally at temperature intervals of 5 K from 283.15 K to 363.15 K and ambient pressure using a precise Anton Paar Digital vibrating-tube densimeter. The apparent molar volumes (Vϕ), thermal expansion coefficient (α) and partial molar volume (V ¯ B) $({\bar V_{\rm{B}}})$ were obtained based on the results of density measurement. The 3D diagram of apparent molar volume against temperature and molality as well as the diagram of thermal expansion coefficient and partial molar volume against molality were plotted, respectively. On the basis of the Pitzer ion-interaction equation of apparent molar volume model, the Pitzer single-salt parameters ( (β M,X (0) v , β M,X (1) v , β M,X (2) v and C M,X v , M X = N a 3 A s O 4) $(\beta _{{\rm{M,X}}}^{(0)v},\beta _{{\rm{M,X}}}^{(1)v},{\rm{ }}\beta _{{\rm{M,X}}}^{(2)v}{\rm{ and }}C_{{\rm{M,X}}}^v,MX = N{a_3}As{O_4})$ and their temperature-dependent correlation F(i, p, T) = a1 + a2ln(T/298.15) + a3(T – 298.15) + a4/(620 – T) + a5/(T – 227) (where T is temperature in Kelvin, ai is the correlation coefficient) for Na3AsO4 were obtained on account of the least-squares method. Predictive apparent molar volumes agree well with the experimental values, and those results indicate that the single-salt parameters and their relational coefficients of temperature-dependence for Na3AsO4 obtained are reliable. [ABSTRACT FROM AUTHOR]

Sodium arsenate, the main component of arsenic‐containing solid waste pollutants, causes serious environmental health threats. Crystallization is one of the effective methods for separating and purifying sodium arsenate from arsenic‐alkali residue lixivium. However, the crystallization process is limited for its low observability and the lack of separation and purification data. In this work, a laser detection system with a magnetic field generator was designed, and the solubility, metastable zone width, interfacial tension, interfacial entropy factor, crystal nucleation, and growth rate of sodium arsenate were investigated in a constant composition environment. The results showed that the solubility, metastable zone width, interfacial tension, and interfacial entropy factor decreases with the presence of a magnetic field. The magnetic field shortened the crystallization induction time and changed the nucleation and growth rate of sodium arsenate. Under the magnetic field, the nucleation rate increased from 2.43 × 1016 to 8.98 × 1017 (s m3)−1, and the growth rate decreased from 4.94 × 10−8 to 2.73 × 10−8 (s m3)−1, the growth mechanism of sodium arsenate as a continuous growth mode was unchanged. In addition, the X‐ray diffraction and infrared showed that the crystal structure of sodium arsenate is unaffected by the magnetic field, indicating that the enhancement of the crystallization process of sodium arsenate with the magnetic field could be a feasible method in engineering application. [ABSTRACT FROM AUTHOR]

Background: Medicinal plants are have been used in the treatment of myriad disease conditions, Alchornea laxiflora is one of such medicinal plant. Aim: To investigate the hepatoprotective effect of hexane root extract of Alchornea laxiflora against sodium arsenate induced liver damage in wistar male rats. Setting and Design: Extraction and administration of bioactive extract. Materials and Methods: Extraction of air-dried ground root of Alchornea laxiflora was done by extracting 500 g with 500 cm of 95% hexane for 72 hrs.The animals (120-150 g) were pre-treated with the extract at varying doses (0.1, 0.5, 1.0, 10, 50 and 100 mg/kg body weight) for seven days orally prior to the intra-peritoneal administration of the toxicant (sodium arsenate) at a dose of 2 mg/kg body weight at the eight day. Hepatoprotective activity of the extracts was evaluated by studying the Cytochrome b5content, Glutathione-S-transferase and 4- Nitroanisole-o-demethylase activities in the liver, Plasma levels of Alanine aminotransferase (AST), Alanine aminotransferase (ALT), Alkaline phosphatase (ALP) and the levels of Total protein, Albumin, Globulin and Glutathione of the various groups. Statistical Analysis: The data were analysed with Microsoft excels (for windows 2007) and Student t-test and ANOVA. Result and Conclusion: The results suggest that pre-treatment of rats with hexane root extract of Alchornea laxiflora for seven days reduced the elevated levels of liver enzymes, reduced the levels of induced liver metabolizing enzymes and the levels of Total protein, Albumin, Globulin and Glutathione that was increased by the toxicity of sodium arsenate in rats and as such possess hepatoprotective effect against sodium arsenate.

Background & Aims: Sodium arsenite, an environmental pollutant, produces free radicals with harmful effects on the reproductive system. The aim of this study was to investigate the effect of curcumin, as a strong antioxidant, on the testis tissue and spermatogenic cell population in mice treated with sodium arsenite. Methods: In this experimental study, Adult male NMRI mice were randomly divided into the 5 groups (n=6): control, sodium arsenite (5mg/kg/day), curcumin (15mg/kg/day), sodium arsenite+curcumin and DMSO as vehicle. After 5 weeks of treatment (through intraperitoneal ingection), animals right testis were removed, fixed, sectioned, stained (using heiden hain azan method) and stereologically studied. Data were analyzed using one-way ANOVA and Tuckey's test and the means were considered significantly different at p

Single crystals of the title compound, Na(H2AsO4), were obtained by partial neutralization of arsenic acid with sodium hydroxide in aqueous solution. The crystal structure of Na(H2AsO4) is isotypic with the phosphate analogue and the asymmetric unit consists of two sodium cations and two tetrahedral H2AsO4− anions. Each of the sodium cations is surrounded by six O atoms of five H2AsO4− groups, defining distorted octahedral coordination spheres. In the extended structure, the sodium cations and dihydrogen arsenate anions are arranged in the form of layers lying parallel to (010). Strong hydrogen bonds [range of O...O distances 2.500 (3)–2.643 (3) Å] between adjacent H2AsO4− anions are observed within and perpendicular to the layers. The isotypic structure of Na(H2PO4) is comparatively discussed.

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Exposure to arsenic, a widespread environmental toxin, produces multiple organ toxicity, including gastrointestinal toxicity. Nigella sativa (NS) has long been revered for its numerous health benefits under normal and pathological states. In view of this, the present study attempts to evaluate the protective efficacy of orally administered Nigella sativa oil (NSO) against arsenic-induced cytotoxic and genotoxic alterations in rat intestine and elucidate the underlying mechanism of its action. Rats were categorized into the control, NaAs, NSO, and NaAs+NSO groups. After pre-treatment of rats in the NaAs+NSO and NSO groups daily with NSO (2 ml/kg bwt, orally) for 14 days, NSO treatment was further continued for 30 days, with and without NaAs treatment (5 mg/kg bwt, orally), respectively. Various biochemical parameters, such as enzymatic and non-enzymatic antioxidants, carbohydrate metabolic and brush border membrane marker enzyme activities were evaluated in the mucosal homogenates of all the groups. Intestinal brush border membrane vesicles (BBMV) were isolated, and the activities of membrane marker enzyme viz. ALP, GGTase, LAP, and sucrase were determined. Further, the effect on kinetic parameters viz K M (Michaelis-Menten constant) and V max of these enzymes was assessed. Integrity of enterocyte DNA was examined using the comet assay. Histopathology of the intestines was performed to evaluate the histoarchitectural alterations induced by chronic arsenic exposure and/or NSO supplementation. Arsenic accumulation in the intestine was studied by inductively coupled plasma-mass spectroscopy (ICP-MS). NaAs treatment caused substantial changes in the activities of brush border membrane (BBM), carbohydrate metabolism, and antioxidant defense enzymes in the intestinal mucosal homogenates. The isolated BBM vesicles (BBMV) also showed marked suppression in the marker enzyme activities. Severe DNA damage and mucosal arsenic accumulation were observed in rats treated with NaAs alone. In contrast, oral NSO supplementation significantly alleviated all the adverse alterations induced by NaAs treatment. Histopathological examination supported the biochemical findings. NSO, by improving the antioxidant status and energy metabolism, could significantly alter the ability of the intestine to protect against free radical-mediated arsenic toxicity in intestine. Thus, NSO may have an excellent scope in managing gastrointestinal distress in arsenic intoxication. [ABSTRACT FROM AUTHOR]

The aim of the study was to compare the effect of sodium arsenate (AsV) on two different cell types: 158N murine oligodendrocytes and HepG2 human hepatoma cells. Exposure of 158N cells to AsV (0.1–400 µM; 48 h) induced a biphasic cytoxic effect defined as hormesis. Thus, low concentrations of AsV stimulate cell proliferation, as shown by phase-contrast microscopy, cell counting with trypan blue, and crystal violet assay, whereas high concentrations induce cell death associated with a loss of cell adhesion. These side effects were confirmed by staining with propidium iodide and cell cycle analysis, characterized by the presence of a subG1 peak, a criterion of apoptosis. The effects of AsV on mitochondrial function, as determined by the 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium (MTT) assay, the measurement of mitochondrial transmembrane potential with 3,3′-dihexyloxacarbocyanine iodide, and the rate of mitochondrial adenosine triphosphate confirm the impact of AsV on the mitochondria. In contrast to 158N cells, HepG2 cells were susceptible to all AsV concentrations as shown by microscopic observations, by counting with trypan blue. However, no alteration is noted in the cell membrane integrity, which indicated an apoptotic mode of cell death, and this side effect is confirmed by the cycle analysis, which revealed a subG1 peak. Of note, there was a loss of MTT, suggesting that AsV induces mitochondrial complex II dysfunction. Altogether, our data show that the cytotoxic characteristics of AsV depend on the cell type considered. [ABSTRACT FROM AUTHOR]

Single crystals of the title compound, Na(H2AsO4), were obtained by partial neutralization of arsenic acid with sodium hydroxide in aqueous solution. The crystal structure of Na(H2AsO4) is isotypic with the phosphate analogue and the asymmetric unit consists of two sodium cations and two tetrahedral H2AsO4- anions. Each of the sodium cations is surrounded by six O atoms of five H2AsO4- groups, defining distorted octahedral coordination spheres. In the extended structure, the sodium cations and dihydrogen arsenate anions are arranged in the form of layers lying parallel to (010). Strong hydrogen bonds [range of O O distances 2.500 (3)-2.643 (3) Å] between adjacent H2AsO4- anions are observed within and perpendicular to the layers. The isotypic structure of Na(H2PO4) is comparatively discussed. [ABSTRACT FROM AUTHOR]

The effects of gibberellic acid (GA3) and sodium arsenate on enzymatic antioxidants activities (superoxide dismutase, guiacol peroxidase and catalase), soluble proteins content, growth and photosynthetic pigments (chl a, chl b, total chl. and carotenoids) of 'Tarom' and 'Shiroudi' rice were investigated. Thirty-days-old seedlings were treated with different concentrations of sodium arsenate (0, 50 and 100 μM) and GA3 (0 and 10 μM) for two weeks. The results showed that sodium arsenate increased the activities of the enzymatic antioxidants and protein content significantly and reduced the growth parameters, chl a, chl b, and carotenoids contents in both cultivars of rice. Meanwhile, GA3 increased the activities of the enzymatic antioxidants, protein content, growth parameters, chl a, chl b, and carotenoids contents significantly in both cultivars of rice treated with sodium arsenate. In general, the results of this study showed that GA3 increased the resistance of the two examined rice cultivars treated with sodium arsenate. [ABSTRACT FROM AUTHOR]

The treatment of microglial BV-2 cells with sodium arsenate (As(V): 0.1–400 μmol/L — 48 hr) induces a dose-dependent response. The neurotoxic effects of high concentrations of As(V) (100, 200 and 400 μmol/L) are characterized by increased levels of mitochondrial complexes I, II, and IV followed by increased superoxide anion generation. Moreover, As(V) triggers an apoptotic mode of cell death, demonstrated by an apoptotic SubG1 peak, associated with an alteration of plasma membrane integrity. There is also a decrease in transmembrane mitochondrial potential and mitochondrial adenosine triphosphate ATP. It is therefore tempting to speculate that As(V) triggers mitochondrial dysfunction, which may lead to defective oxidative phosphorylation subsequently causing mitochondrial oxidative damage, which in turn induces an apoptotic mode of cell death. [ABSTRACT FROM AUTHOR]

Arsenic residue is of great concern due to its environmental hazard. In this study, we first propose to use cullet as the host to immobilize sodium arsenate. All samples have successfully formed glasses in 1200 °C detected by X-ray diffraction spectra (XRD). High arsenic immobilization ratio has been achieved in the experiment. Fourier transform infrared spectrometer (FTIR) and X-ray photoelectron spectroscopy (XPS) have been used to explore the process of arsenic immobilized into the cullet. It can be concluded that the arsenic exists in the form of AsO 4 tetrahedron and forms chemical bonds with SiO 4 tetrahedron via bridging oxygen, resulting in strengthening the Q n structure and new formation of Si-O(BO)-As, which makes arsenic stable in the glass. [ABSTRACT FROM AUTHOR]

Background & Aims: Sodium arsenite, an environmental pollutant, produces free radicals with harmful effects on the reproductive system. The aim of this study was to investigate the effect of curcumin, as a strong antioxidant, on the testis tissue and spermatogenic cell population in mice treated with sodium arsenite. Methods: In this experimental study, Adult male NMRI mice were randomly divided into the 5 groups (n=6): control, sodium arsenite (5mg/kg/day), curcumin (15mg/kg/day), sodium arsenite+curcumin and DMSO as vehicle. After 5 weeks of treatment (through intraperitoneal ingection), animals right testis were removed, fixed, sectioned, stained (using heiden hain azan method) and stereologically studied. Data were analyzed using one-way ANOVA and Tuckey's test and the means were considered significantly different at p<0.05. Result: A significant decrease in the mean volume (P<0.05) and diameter (P<0.001) of seminiferous tubules, height of the germinal epithelium (P<0.01), thickness of the basement membrane (P<0.001) and the number of spermatocytes and spermatids (p<0.001) and a significant increase in the mean volume of the interstitial tissue was observed in the sodium arsenite group compared to the control ones (p<0.05). The above parameters were significantly compensated to the control level in the sodium arsenite+curcumin group. Conclusions: Curcumin can compensate the harmful effects of sodium arsenite on the testicular tissue and spermatogenic cell populations in adult mice. Therefor, it is suggested as a supplement in the case of arsenite intoxication. [ABSTRACT FROM AUTHOR]

We found a unique property of E. coli purine nucleoside phosphorylases to selectively perform the arsenolysis reaction of ribonucleosides in their active site without affecting β-D-arabinonucleosides. In the synthesis of modified β-D-arabinonucleosides from the corresponding ribonucleosides, the catalytical amount of sodium arsenate in the transglycosylation reaction provided a 95 to 98% conversion rate. Such an approach was shown to simplify the composition of the reaction mixtures and facilitate the isolation of the target nucleosides, particularly, vidarabine, fludarabine, and nelarabine. [ABSTRACT FROM AUTHOR]