The present study was planned to evaluate the protective role of resveratrol (Res) against subchronic malathion exposure in rats over four weeks. In total, 48 Wistar rats were used and divided equally into six groups. The groups were designed as the control group (received only a rodent diet and tap water), the corn oil group (0.5 ml corn oil by the oral route), and the malathion group (100 mg kg day by the oral route). Other three groups received malathion (100 mg kg day) plus Res (5, 10, and 20 mg kg day, respectively) by the oral route. Malathion increased malondialdehyde and 8-OHdG levels, whereas it decreased glutathione levels. Also, acetylcholinesterase, superoxide dismutase, and catalase activities were found to be low in the blood, liver, kidney, heart, and brain tissues. Biochemical parameters were not notably changed in all groups. In contrast, Res treatment inverted malathion-induced oxidative stress, lipid peroxidation, and activity of enzymes. Additionally, malathion-induced histopathological changes in the liver, kidney, heart, and brain were ameliorated by Res treatment. These results demonstrate that malathion increases oxidative stress and decreases the antioxidant status while Res has a protective function against malathion toxicity in rats.

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Organophosphorus compounds cause oxidative stress and lead to alterations in antioxidant status in organisms. In this study, the effects of subchronic exposure to malathion and the protective effects of boron (B) were evaluated in 48 Wistar rats, which were divided equally into six groups. For 28 d, the control group received a normal diet and tap water, the corn oil group received a normal diet and 0.5 mL of corn oil by gastric gavage and the malathion group received a normal diet and malathion (100 mg/kg/d) by gastric gavage. During the same period, each of the three other groups received a different dosage of B (5, 10 and 20 mg/kg/d, respectively) and malathion (100 mg/kg/d) by gastric gavage. Malathion administration during the period increased malondialdehyde, nitric oxide and 8-hydroxy-2'-deoxyguanosine (8-OHdG) levels, as well as markers of liver function, yet decreased acetylcholinesterase, reduced glutathione, superoxide dismutase, and catalase activities in blood, liver, kidney and brain tissues. Administration of B in a dose-dependent manner also reversed malathion-induced oxidative stress, lipid peroxidation (LPO) and antioxidant enzyme activity. Moreover, B exhibited protective action against malathion-induced histopathological changes in liver, kidney and brain tissues. These results demonstrate that, if used in a dose-dependent manner, B decreases malathion-induced oxidative stress, enhances the antioxidant defense mechanism and regenerates tissues in rats.

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Boron reversed Bisphenol-A induced alterations.

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