The effects of subchronic methidathion toxicity on rat liver: Role of antioxidant vitamins C and E

Abstract

Methidathion (MD) phosphorodithioic acid S-[(5-methoxy-2-oxo-1,3,4-thiadiazol-3(2H)-yl)methyl] O,O-dimethyl ester is the organophosphate insecticide (OPI) most commonly used worldwide in the pest control of crops. Subchronic MD exposure was evaluated for its effects on lipid peroxidation, the serum activities of cholinesterase (ChE), and enzymes concerning liver damage, and the protective effects of combination of vitamins E and C in albino rats. Additionally, the histopathological changes in liver tissue were examined. Experimental groups were as follows: control group; a group treated with 5 mg/kg body weight MD (MD group); and a group treated with 5 mg/kg body wight MD plus vitamin E plus vitamin C (MD+AO group). The MD and MD+AO groups were treated orally with MD on five days a week for 4 weeks. The serum activities of cholinesterase (ChE), alanine transferase (ALT), aspartate amiotransferase (AST), lactate dehydrogenase (LDH), gamma-glutamyltransferase (GGT), alkaline phosphatase (ALP), and the concentration of malondialdehyde (MDA) and liver histopathology were studied. In serum samples, MD significantly increased MDA concentration and ALP, AST, GGT, LDH activities but decreased the ALT and ChE activities. In the MD+AO group, MDA level and ALP, AST, LDH activities were significantly decreased and ChE activity was increased compared to the MD group. Histopathological changes found in liver tissue of rats treated with MD included were infiltration with mononuclear cells in all portal areas, sinusoidal dilatation, and focal microvesicular steatosis and hydropic degenerations in parenchymal tissue. The severity of these lesions was reduced by administration of vitamins. From these results, it can be concluded that subchronic MD causes liver damage, and lipid peroxidation may be a molecular mechanism involved in MD-induced toxicity. Furthermore, the combination of vitamins E and C can reduce the toxic effects of MD on liver tissue of rats.

Methidathion-induced hematological, biochemical and hepatohistological alterations in rat: Ameliorative effects of selenium and zinc

“…These observations possibly come from the toxic effects of generated reactive oxygen species which upset the liver membrane components. Similarly, OP-treated rats have experienced almost the same perturbations including inflammation, and hepatocellular degeneration (Gokalp et al, 2003;Kalender et al, 2010;Sutcu et al, 2006). However, the co-treatment of Se plus Zn has reduced the histological alterations induced by MD, which might be attributed to their antiradical/antioxidant roles.…”

“…Only corn oil was given in the same way to the control group. The dose of MD used in this study represents 1/15 of LD50 (5 mg/kg bw) which has been used previously by other investigators since it is toxic but not lethal to rats (Sutcu et al, 2006;Güney et al, 2007). The doses of Na2SeO3 and ZnSO4 were selected based on the clinical application and on results from previous experiments in human and experimental animals against heavy pesticide poisoning (Goel et al, 2005;Mansour and Mossa, 2009;Ben Amara et al, 2011).…”

The Effect of Methidathion on Sex Hormones, Sperm Parameters and Testicular Tissue in Mice

“…Pesticide are hydrophobic molecules that bind widely to biological membranes, essentially phospholipid bilayers [27] , and they may cause damage to the membranes by generate lipid peroxidation. [26] Previous studies have reported that methidathion caused oxidative damage by lipid peroxidation in rat aortic wall, heart tissue, liver and ovary [28,12,8,15]. [29] have shown that single-dose treatment with methidathion increases lipid peroxidation in rat erythrocytes.…”

“…[29] have shown that single-dose treatment with methidathion increases lipid peroxidation in rat erythrocytes. [8] have shown lipid peroxidation may be a molecular mechanism contributory in methidathion induced toxicity. lipid peroxidation occur through the generation of reactive oxygen species (ROS) that may be produced as a result of methidathion metabolism or due to high energy consumption to inhibit oxidative phosphorylation.…”

“…[6] However, the frequent use of OP pesticide and accessibility have increased their risk. [7] MethidathionS-(2,3-Dihydro-5-methoxy-2-oxo-1,3,4-thiadiazol-3-ylmethyl) O,O-dimethyl phosphorodithioate, is one of the most widely OP pesticide used in the world for pest control of crop [8] , The department of pesticide regulation (DPR) Environmental Protection Agency placed methidathion on high-priority roster for risk and its value based on the conceivable adverse effects in chronic toxicity, carcinogenesis and chromosomal anomalies. [9] Methidathion and the substances produced by the metabolite within the body of organism their toxic reaction primarily through their irreversible inhibition of cholinesterase (ChE) enzymes [10,9] , the main way to metabolize methidathion in liver was through glutathion-stransferase and the primary metabolizer was desmethylmethidathion.…”