Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.6.3.1 (Mg2+-ATPase)
 1,484 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Endosulfan (E) is an organochloric insecticide, which is quickly metabolized and eliminated from the body system. Toxic effects of E and its metabolites have been reported. The influence of E and its metabolites, viz. endosulfan sulfate (ES), endosulfan diol (ED) and endosulfan lactone (EL), has been examined on rat liver mitochondria in vitro. Endosulfan stimulated state-4 respiration at lower concentrations and inhibited it at higher ones, whereas state-3 respiration was inhibited at all the concentrations used, i.e. 5-100 micrograms/ml. A maximal 25-fold activation of latent Mg2+-ATPase was achieved at a concentration that caused maximal stimulation of state-4 respiration. Activities of the respiratory chain-linked enzymes were inhibited at levels which corresponded to the concentrations of endosulfan used in vitro. Both the respiratory control ratio (RCR) and the ADP:O ratio fell sharply at endosulfan concentrations above 10 micrograms/ml. ES and ED exerted similar effects on mitochondrial oxidation of beta-hydroxybutyrate, but at more than double the concentration of the parent compound, while EL proved least effective. The effects of the latter compound on mitochondrial enzyme activities were negligible. Our results suggest that endosulfan possesses dual properties, that of an uncoupler of oxidative phosphorylation and of an inhibitor of the electron transport chain, and that the in vivo cytotoxic/insecticidal effects of endosulfan and its metabolites might, therefore, be the consequence of impaired mitochondrial bioenergetics.
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PMID:Effects of endosulfan and its metabolites on rat liver mitochondrial respiration and enzyme activities in vitro. 614 50

Arsenic is a known global groundwater contaminant. The organochlorine insecticide endosulfan has gained significance as an environmental pollutant due to its widespread use in the control of many food- and non-food-crop-damaging insects. The adverse effects produced by arsenic or endosulfan alone in humans and animals are well documented, but very little is known about the consequences of their coexposure. We evaluated whether their simultaneous exposure can induce oxidative stress and affect antioxidative systems and certain membrane-bound enzymes in erythrocytes of broiler chickens. Day-old chicks were exposed to 3.7 ppm of arsenic via drinking water or 30 ppm of endosulfan-mixed feed or similarly coexposed to these in the same dose levels for 60 days. At term, the impact of their coexposure was assessed by evaluating lipid peroxidation (LPO), activities of superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), glutathione-S-transferase (GST), different ATPases and acetylcholinesterase (AChE) in erythrocytes, serum glucose, and levels of glutathione (GSH) and glycosylated hemoglobin (GHb) in blood. LPO was increased with all of the treatments. Catalase was decreased with endosulfan and the coexposure, but not with arsenic, whereas GSH was decreased with arsenic and endosulfan, but not with the coexposure. All of the treatments increased SOD and GPx activities. GST activity was increased only in the coexposed birds. None of the treatments affected the activities of total ATPase and Mg2+-ATPase. Na+-K+-ATPase activity was decreased in the endosulfan-treated and the coexposed birds. All three exposures increased erythrocyte AChE activity. Endosulfan increased the serum glucose level and arsenic and endosulfan increased GHb levels, but these were not altered in the coexposed birds. Erythrocyte protein content was insignificantly decreased with these treatments. Overall, the effects of coexposure were not appreciably different from either of the agents, except on AChE, GSH, and glucose. The results do not reflect any specific type of interaction between these agents in chicken erythrocytes, but they do indicate that the coexposure induces a low level of oxidative stress, which is comparable to that induced by arsenic or endosulfan.
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PMID:Effects of subchronic coexposure to arsenic and endosulfan on the erythrocytes of broiler chickens: a biochemical study. 1844 43