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This study focused on organophosphate malathion toxicity in Danube sturgeon (Acipenser gueldenstaedtii) and its negative effects in sub-lethal concentration. In this context, the LC50 value of fish exposed to five different concentrations and two different sub-lethal concentrations depending on the LC50 value were considered. Accordingly, LC50 of malathion for 96 h was 3.24 mg L-1. In leukocyte (WBC) and hemoglobin (HGB) such as hematological indicators, significant differences were observed in sub-lethal concentration (One-eighth of the LC50 =0.4 mg L-1). In addition, serious histological alterations were observed in the gill and liver tissues after both acute (96 h) and chronic periods (28 days). While epithelial lifting and hyperplasia were the most prominent lesions in the gill, intense vacuolization were observed in the liver. In addition, circulatory disturbances, regressive changes, and progressive changes in the gill and circulatory disturbances and inflammation in the liver were significantly higher for the chronic period. Finally, significantly higher DNA damage was detected in fish exposed malathion in the chronic period compared to the control group. In conclusion, the present study has proven that malathion has a hematological, histological and genotoxic effect on the endangered species A. gueldenstaedtii. Thus, the current study will motivate for residue studies on A. gueldenstaedtii and trigger conservation strategies for local governments. • Malathion, which is used extensively as a pesticide, has a toxic effect on Danube sturgeon. • Hematological negative results were observed after malathion exposure. • Malathion caused histological adverse effects on the gill and liver tissues of fish. • Based on DNA damage analysis, malathion has genotoxic impact on Danube sturgeon. [ABSTRACT FROM AUTHOR]

Highlights • Effects of malathion exposure were studied on cultured porcine granulosa cells. • Malathion increased ROS levels and activated the antioxidant defense system. • Malathion caused DNA damage, apoptosis and autophagy. Abstract Malathion is a wide spectrum organophosphorothionate insecticide that is frequently found in drinking water, food and foodstuffs. Ovarian granulosa cells modulate oogenesis by providing metabolic nutrients to oocytes. They can decide the fate of folliculogenesis and oocyte maturation by supplying regulatory cues that help in reproduction. However, little is known about the underlying mechanisms of malathion as a reproductive toxicant in porcine granulosa cells. In the present study, we found that malathion has obvious toxic effects on cultured porcine granulosa cells in a dose-dependent manner. Malathion exposure resulted in significantly increased oxidative stress levels and DNA damage response, which was measured by the mRNA expression levels of homologous recombination (HR) pathway and non-homologous end-joining (NHEJ) pathway-related genes. Subsequently, it was found that malathion exposure could induce apoptosis and autophagy by qRT-PCR and fluorescence intensity analysis. In conclusion, malathion is a reproductive toxicant by inhibiting granulosa cell proliferation by multiple pathways connected to oxidative stress, DNA damage, apoptosis and autophagy. [ABSTRACT FROM AUTHOR]

Pesticides are being used globally to improve agricultural production. They are applied specifically to combat with pathogens that are a major threat for reduced optimum yield of crops. This study was carried out to see the effect of commercially used pesticides on a specific plant protein viz. phytocystatin isolated from yellow mustard seeds (YMP). Phytocystatin is a thiol proteinase inhibitor, which regulates endogenous and exogenous cysteine proteinases and plays a vital physiological role in plants. Different classes of pesticides like fungicide (iprodione) of dicarboximide class and an insecticide (malathion) of class organophosphate are retorted for our study. In the presence of these pesticides, biophysical and biochemical changes were observed in phytocystatin. These changes were evaluated making use of caseinolytic activity assay, UV–vis spectroscopy, fluorescence spectroscopy, FTIR, and circular dichroism. Isothermal titration calorimetry was employed to see interaction pattern of these pesticides with phytocystatin. The results obtained clearly depict that the pesticides bind with the phytocystatin thereby changing its native conformation and reducing its intrinsic property of inhibition on cysteine proteinase as evident by reduced anti-papain inhibition in the presence of pesticides. Furthermore, CD and FTIR spectroscopy results clearly show a decrease in α-helical content upon interaction with malathion and iprodione. Among the two pesticides, iprodione has far more pronounced effect on YMP evident from striking changes in UV, Fluorescence, CD and FTIR spectroscopy. 2,4-dinitrophenylhydrazine spectrophotometric assay was also carried out to check production of ROS, generation of ROS was observed in the presence of these pesticides thus implying that ROS might be responsible for changes in native structure of phytocystatin induced by pesticides. [ABSTRACT FROM AUTHOR]

Studies indicate that the pesticide malathion may have a role in diabetes. Herein, we determined the effects of different concentrations of malathion on survival, ultrastructure, and electrophysiologic islet cell parameters. Acutely, high concentrations of malathion (0.5 or 1 mM) increased cell death in rat islet cells, while low concentrations (0.1 mM) caused signs of cell damage in pancreatic α and β cells. Exposure of RINm5F cells to malathion for 24 or 48 h confirmed the reduction in β-cell viability at lower concentrations (0.001–100 µM). Chronic exposure of mouse pancreatic α and β cells to 3 nM of malathion led to increased voltage-gated K+ (K v) currents in α-cells. Our findings show a time and concentration dependency for the malathion effect on the reduction of islet cell viability and indicate that pancreatic α cells are more sensitive to malathion effects on K v currents and cell death. [Display omitted] • Malathion causes degeneration of the basement membrane in rat pancreatic islets. • Malathion exposure leads to increased cell death in rat pancreatic islets. • Malathion increases autophagy and cell death in pancreatic rat α and β cells. • Immortalized RINm5F cells exposed to malathion have reduced cell viability. • Malathion causes increased K+ currents in mouse α cells but not in β cells. [ABSTRACT FROM AUTHOR]

Toxicity resulting from off-target effects, beyond acetylcholine esterase inhibition, for the commonly used organophosphate (OP) insecticides chlorpyrifos (CPS) and malathion (MA) was investigated using Saccharomyces cerevisiae and Caenorhabditis elegans model systems. Mitochondrial damage and dysfunction were observed in yeast following exposure to CPS and MA, suggesting this organelle is a major target. In the C. elegans model, the mitochondrial unfolded protein response pathway showed the most robust induction from CPS and MA treatment among stress responses examined. GABAergic neurodegeneration was observed with CPS and MA exposure. Impaired movement observed in C. elegans exposed to CPS and MA may be the result of motor neuron damage. Our analysis suggests that stress from CPS and MA results in mitochondrial dysfunction, with GABAergic neurons sensitized to these effects. These findings may aid in the understanding of toxicity from CPS and MA from high concentration exposure leading to insecticide poisoning. [Display omitted] • Mitochondrial stress appears to be a major off-target effect of CPS and MA. • Stress from CPS and MA causes neurodegeneration of GABAergic neurons C. elegans. • DAergic and cholinergic neurons are not significantly damaged by CPS and MA. • Behavior analysis of CPS and MS exposed worms suggests motor neuron damage. • Off-target effects of CPS and MA in models may be relevant to human exposure. [ABSTRACT FROM AUTHOR]

Malathion has a broad range of toxicities while its reproductive effects have not been fully elucidated. In this study, we treated animals with malathion by gavage at doses of 0, 33.75, 54, and 108 mg/kg for 60 days and evaluated the alterations in histology, biochemistry and serology. Malathion caused the reduction in the sperm counts and motility. The reduced body and testis weights were coupled with mild to severe degenerative changes in seminiferous tubules. We found malathion at 54 mg/kg increased spermatogenic apoptosis rate which was confirmed by changes in protein expression of Bax and Bcl-2. The activities of testicular enzymes including ACP, LDH and γ-GT were significantly altered with the reduced level of reproductive hormones such as LH, FSH and T. These results indicate that malathion can elicit deleterious effects on reproductive system of rats. The abnormal levels of hormones and apoptotic proteins induced by malathion may play important roles. [ABSTRACT FROM AUTHOR]

Insulin resistance and risk of type 2 diabetes are the most important complications following exposure to organophosphorous (OPs) pesticides. Regarding the importance of liver on metabolic pathways regulation, in particular blood glucose homeostasis, we focused on liver inflammation and oxidative damages in a subchronic model of toxicity by malathion. Adult male Wistar rats of body weight 200–250 g were used for the study. Malathion (200 mg/kg b.w./day) was administered to rats by oral intubation for 28 days. Glycemic and insulin resistance indices, markers of liver injury, markers of inflammation and oxidative stress were assessed. Malathion-treated rats showed increased glycemia, insulinemia and glycated hemoglobin level, HOMA-IR and HOMA-β indices, plasma activities of hepatocellular enzymes, lipid peroxidation index, CD3 + /CD4 + and CD3 + /CD4 + and pro-inflammatory cytokines when decreased antioxidant status in liver was noted. Most of our study indicates that malathion promotes insulin resistance, inflammation and Hepatosteatosis in subchronic model of exposure. On the basis of biochemical and molecular findings, it is concluded that insulin resistance induced by malathion occurs through oxidative stress and related pro-inflammatory markers in a way to result in a reduced function of insulin in liver cells. [ABSTRACT FROM AUTHOR]

Neuroblastoma is primarily an embryonal tumor of infancy. Recently, some toxicological agents used as pesticides have been associated with an increased incidence of this tumor. We intended to determine the potential association between prenatal exposure to pesticides and the incidence of neuroblastoma in children. Studies targeting the link between neuroblastoma and pesticides were searched in PUBMED, SCOPUS, and Google Scholar from January 1, 1960, through December 2020. We performed a PRISMA-based systematic review and meta-analysis. In addition, we took into consideration the IARC evaluation on pesticides issued in recent monographs. Prenatal pesticide exposure is associated with an increased risk of neuroblastoma with an OR of 1.6 (1.1–2.3; p = 0.013), while the OR is 1.0 (0.8–1.3; p = 0.723) for pesticide exposure after birth. There is a significant association between prenatal pesticide exposure and neuroblastoma. We emphasize the IARC conclusions evaluating the carcinogenicity of diazinon, glyphosate, malathion, parathion, and tetrachlorvinphos. [Display omitted] • Neuroblastoma is an embryonal tumor with an increased rate in the last decades. • Pesticide's widespread use may have played a role in some tumors of childhood. • Parental exposure to pesticides may be linked to the increased rate of this tumor. [ABSTRACT FROM AUTHOR]

Highlights: [•] Endosulfan treated catfish testis show differential expression in proteins like ubiquitin and Esco2. [•] Melanocortin-receptor-2/ACTH receptor is upregulated in endosulfan treated ovary. [•] Prolactin is upregulated in malathion treated catfish ovary. [•] Differentially expressed proteins in gonads due to pesticide exposure might indicate reproductive impairment as a consequence. [Copyright &y& Elsevier]

Highlights: [•] Dose-dependent inhibition of AChE activity after exposure to investigated insecticides. [•] Recorded additive effect for mixtures of endosulfan with malathion and endosulfan with pirimiphos-methyl. [•] Recorded additive effect for mixtures of temephos with malathion and temephos with pirimiphos-methyl. [•] Recorded synergistic effect for mixture of endosulfan and temephos. [•] Indicated antagonistic effect for mixture of malathion and pirimiphos-methyl. [ABSTRACT FROM AUTHOR]

Abstract: The organophosphorus (OP) pesticide malathion is a highly neurotoxic compound. Some studies have reported neurotoxicity signs after in utero exposure to OP pesticides. However there is no evidence of the exclusive contribution of the lactational exposure to malathion as a possible cause of neurotoxicity in rats’ pups. In this respect, we investigated the exclusive contribution of malathion (200mg/kg, b.w.) exposure through maternal milk in rat pups during lactation. We evaluated the activity of acetylcholinesterase (AChE) and butyrylcholinesterase (BChE), as well as on biochemical parameters related to the oxidative stress such lipoperoxidation and antioxidant enzyme activities as superoxide dismutase (SOD) and catalase (CAT) in the brain, plasma and erythrocytes of rats’ pups at 21st postnatal day (Pnd). These parameters were also evaluated in the same tissues but at 51 Pnd. Our results showed that the malathion exposure during lactation induced a high inhibitory effect of the brain, plasma and erythrocyte AChE and BChE activities in rat pups. Many changes were observed in the biochemical parameters related to the oxidative stress for pups brain, plasma and erythrocyte. The present study shows, for the first time, that the exposure of postnatal pups to malathion via lactation inhibits the activity of brain, plasma and erythrocytes cholinesterase in the pups. These findings suggest that malathion exposure during lactation induced a cerebral alterations and oxidative stress in rat pups. [Copyright &y& Elsevier]

Abstract: Groundwater contamination with arsenic is a major global health concern. The organophosphorus insecticide malathion has gained significance as an environmental pollutant due to its widespread use in agriculture, grain storage, ectoparasite control and public health management. The deleterious effects produced by arsenic or malathion alone are documented, but very little is known about the consequences of their coexposure. The aim of the current study was to examine the effects of repeated simultaneous exposure to arsenic and malathion on drug-biotransforming enzymes in the liver of broiler chickens. One-month-old broiler chickens were exposed daily to arsenic (50ppm)-supplemented drinking water, malathion (500ppm)-mixed diet or in a similar fashion coexposed to these agents for 28 days. At the term, changes in body weight, organ weights, and levels of hepatic cytochrome P450 (CYP), cytochrome b 5 , microsomal and cytosolic proteins; aminopyrine N-demethylase (ANDM), aniline P-hydroxylase (APH), glutathione S-transferase (GST) and uridine diphosphate glucuronosyltransferase (UGT) were assessed. Arsenic, malathion or their coexposure decreased the body weight gain and liver weight. Brain weight (relative) was increased with arsenic or malathion, but not with the coexposure. Treatment with arsenic decreased the CYP and cytochrome b 5 contents by 39 and 36%, than with malathion by 54 and 22% and the coexposure by 45 and 28%, respectively. The ANDM activity was decreased with arsenic (44%), malathion (23%) and the coexposure (32%). Arsenic (23%) and the coexposure (37%), but not malathion (14%), reduced the APH activity. The activities of hepatic microsomal and cytosolic GST were increased with all the three treatments [Arsenic (microsomal: 88% cytosolic: 113%), malathion (microsomal: 137%, cytosolic: 94%) and coexposure (microsomal: 140%, cytosolic: 148%)]. These treatments did not significantly affect the hepatic UGT activity, but reduced the hepatic microsomal (arsenic: 28%, malathion: 34% and coexposure: 43%) and cytosolic (17–19%) protein contents. The effects of coexposure on the activities of various phase I and phase II drug-biotransforming enzymes were almost similar to that of arsenic or malathion. This study provides evidence that repeated coexposure to arsenic and malathion may influence the extent of drug metabolism in chickens. [Copyright &y& Elsevier]

Malathion is an insecticide of the group of organophosphate pesticides (OPs), which shows strong insecticidal effects. However, it possesses mutagenic and carcinogenic properties and shows organ-specific toxicity in relation to the heart, kidney and other vertebrate organs. The exact mechanism of the genotoxic effects of malathion is not yet known. Free radical damage is an important direct or indirect factor in several pathological and toxicological processes, including malathion poisoning. The aim of the present study was the evaluation of oxidative damage in different tissues of Wistar rats, administered intra peritoneally at doses of 25, 50, 100 and 150mgmalathion/kg, after acute and sub-chronic malathion exposure. Oxidative stress evaluation was based on lipid peroxidation by levels of thiobarbituric acid reactive substances (TBARS), protein oxidation by levels of carbonyl groups, and also on the activities of superoxide dismutase and catalase, two antioxidant enzymes that detoxity superoxide radical (O2 −) and hydrogen peroxide, respectively. The results showed that the most sensitive targets of oxidative damage were kidney, lung and diaphragm after acute treatment, and liver, quadriceps and serum after sub-chronic treatment. Also, in general, increased lipid peroxidation measured as TBARS levels seems to be a better biomarker of oxidative stress compared to the contents of protein carbonyls after acute and sub-chronic malathion treatments. The present findings reinforce the concept that oxidative stress and particularly lipoperoxidation, are involved in OPs toxicity. [Copyright &y& Elsevier]

Abstract: The objective of this study was to establish an accurate in vitro model for cutaneous absorption in anurans. The harvested perfused anuran pelvic limb (HPAPL) model maintains the anatomic and physiologic integrity of the skin from the pelvic limb, including the intact capillary network. Radiolabeled malathion was applied to the skin of the dorsal thigh, and perfusate was collected over a 6h period. Residues from the skin surface, stratum externum, and dosed area beneath the stratum externum were analyzed. Kinetic parameters were calculated from these data. Absorption was significantly less for the HPAPL than previously reported for Teflon flow-through diffusion cells. However, partitioning effects were comparable. The HPAPL is an appropriate in vitro model for examining cutaneous absorption kinetics in the bullfrog. [Copyright &y& Elsevier]

Abstract: Malathion is one of the most extensively used organophosphorus pesticides applied in agriculture, mosquito eradication and in the control of animal ectoparasites and human body lice. The widespread use of malathion has raised concern over its potential to cause untoward health effects in humans, animals and birds. Malathion inhibits cytochrome P450 monooxygenases and has the potential to alter pharmacokinetic profiles of therapeutic agents that are metabolized in the liver. The present study was undertaken to evaluate the impact of subchronic exposure of malathion on the pharmacokinetic disposition of pefloxacin. Chickens were given either normal diet or malathion through food at a concentration of 1000ppm for 28 days. Subsequently, pefloxacin was administered either intravenously or orally (control) to birds fed normal diet and orally to malathion-exposed chickens at a dosage of 10mgkg−1 body weight. Blood samples were drawn from the brachial vein at predetermined time intervals after drug administration. Plasma was separated and analyzed for pefloxacin by reverse-phase high performance liquid chromatography. The plasma concentration–time data were analyzed by non-compartmental techniques. Following intravenous administration of pefloxacin, elimination half-life (t 1/2β ), area under the plasma concentration–time curve (AUC) and mean residence time (MRT) were 8.2±0.7h, 66±9μghml−1 and 10.5±1.1h, respectively, and when the drug was administered orally, the respective values of pharmacokinetic parameters were 8.2±0.4h, 31±3.1μghml−1 and 11.7±0.6h. Malathion exposure significantly increased maximum plasma drug concentration, t 1/2β , AUC and MRT of pefloxacin to 54, 22, 117 and 37% of control, respectively. These findings provide evidence that subchronic malathion exposure markedly influences the elimination kinetics of pefloxacin which may be due to malathion-mediated inhibition of metabolism of pefloxacin. [Copyright &y& Elsevier]

Abstract: Organophosphorus compounds such as malathion are environmental contaminants that may evoke neurobehavioral responses including anxiety and depression. In this study, after a functional observational battery, rats were tested in an open field and temperature test to better define doses used in subsequent experiments. Then, we investigated the effects of acute and repeated treatment with malathion on elevated plus-maze and forced-swim test, which are validated animal models to observe for anxiety- and depressive-related behaviors, respectively. We found that both acute and repeated malathion administration induced anxiogenic and depressive-like responses at doses that affected neither locomotion nor systemic temperature. Biochemical assays demonstrated inhibition of cholinesterase activity by these effective doses. [Copyright &y& Elsevier]

Abstract: Regarding the widespread use of organophosphorous pesticides (OP) especially malathion in environment and reported cases of muscle disturbances in human and animal, the present work was undertaken to explore effects of malathion subchronic exposure on rat leg skeletal muscle glucose metabolism by measuring key enzymes of glycogenolysis and glycolysis. Malathion was administered through food for 4 weeks at concentrations of 100, 200, and 400ppm to rats. Activities of enzymes including glycogen phosphorylase (GP), hexokinase (HK), and phosphofructokinase-1 (PFK) were measured in skeletal muscle homogenate of exposed rats. Levels of glucose and insulin were measured in blood. Four weeks administration of malathion at doses of 200 and 400ppm increased blood glucose concentrations to 44.4 and 60.6% of control, respectively. Malathion at doses of 200 and 400ppm increased blood insulin concentration to 36.6 and 143.2% of control, respectively. Malathion at doses of 100, 200, and 400ppm increased muscle PFK activity to 40.4, 53.5, and 83.1% of control, respectively. Malathion at doses of 400ppm increased skeletal muscle GP to 91.6% of control. Skeletal muscle HK was not influenced by malathion treatment. It is concluded that malathion influences muscle glycogenolysis and glycolysis as well as secretion of insulin from pancreas which all may explain diabetic potential of malathion. [Copyright &y& Elsevier]

A mixture of malathion (4%), carbaryl (2%) and cypermethrin (4%) was applied as dry powder to forest and grasslands at a rate of 5kg/ha for tick control in 1500ha of a deer hunting estate in the south of Spain. The effect on plasma cholinesterase (ChE) of house sparrow and nightingale, and brain ChE of red-legged partridge was studied. Plasma ChE was lower after the treatment in passerine birds, but brain AChE was not affected in partridges. The body condition of house sparrows was significantly lower after the treatment. [Copyright &y& Elsevier]