The present study was planned aiming to investigate the effects of atrazine herbicide exposure on stress biomarkers acetylcholinesterase activity (AchE) and cortisol, oxidative stress responses and the histopathological changes in liver of female Clarias gariepinus and the ameliorative effect of vitamin E supplementation (240mg/kg diet) on the degree of atrazine sublethal toxicity (1.37mg/l) for 6 weeks. Chronic exposure to atrazine revealed a marked inhibition in the activity of AchE. But, significant increase of serum cortisol level was recorded. Moreover, atrazine exposure was associated with a marked induction of oxidative damage in liver tissue as evidenced by increased level of lipid peroxidation (LPO) and reduced glutathione (GSH) content. Atrazine exposure also led to a significant increase in the activities of catalase (CAT) and superoxide dismutase (SOD).Furthermore, histopathological examination of the liver of exposed fish showed dilatation and congestion of blood vessels, fatty degeneration, necrosis and pyknotic nuclei of hepatocytes. However, fish fed diet supplemented with vitamin E exhibited protective effect by minimizing the atrazine-induced toxicity, through measured values more or less similar to the control group fish.

The present study was planned to investigate the effect of methomyl or imidacloprid on the brain of male rats. The effect grape seeds oil as an antioxidant was also evaluated. Animals were administered orally with 1/10 and 1/20 of LD 50 methomyl and imidacloprid with 17 and 450 mg /kg bw for four and eight weeks. Grape seeds oil with 4 ml/kg b.wt. was used for protection from methomyl and imidacloprid toxicity. Brain cortex and hippocampus oxidative stress (glutathione S transferase GST, glutathione peroxidase GPX, superoxide dismutase SOD, malondialdhyde MDA and nitric oxide NO), Na + ,K + , ATPase and acetylcholinesterase AChE were determined. The result showed that GST, GPX, MDA, and NO 2 were increased significantly. But SOD, Na + K + ATPase and AChE were significantly reduced in comparison with the control. Grape seed oil induced a significant improvement for the pesticides brain toxicity but not to the level of control. The study suggested that the oil antioxidants not improve the brain toxicity induced by methomyl or imidacloprid.

OBJECTIVES:To study the effect of oral administration of grape seed oil (GSO) against carbontetrachloride (CCl4)-induced hepatotoxicity in rat Liver damage was induced in male Wistar rats (150-200 g) by administering CCl4 (0.5 ml/kg, i.p.) once per day for 7 days and the extent of damage was studied by assessing biochemical parameters such as alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) in serum and concentrations of glutathione (GSH), superoxide dismutase (SOD), and total protein (TP) in liver. The effect of coadministration of GSO (3.7 g/kg, orally) on the above parameters was further investigated and compared with a vitamin E (100 mg/kg, orally) treated group. RESULTS: Oral administration of GSO (3.7 g/kg, body weight orally) for 7 days resulted in a significant reduction in serum AST, ALT, and ALP levels and significant improvement in glutathione, SOD, and TP, when compared with CCl4 damaged rats. The antioxidant effect of GSO at 3.7 g/kg for 7 days was found to be comparable with vitamin E (100 mg/kg, orally) in CCl4-treated rats. CONCLUSION: The GSO has protected the liver from CCl4 damage. Probable mechanism of action may be due to the protection against oxidative damage produced by CCl4.

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