Rutin is a flavonoid present in many plant species. Because of its antioxidant, anti‐inflammatory, and antiapoptotic properties, rutin is of interest for its potential protective effects against toxic agents. The hepatoprotective, renoprotective, and cardioprotective effects of rutin are reviewed. The antioxidant effects of rutin are elicited by enhancing antioxidant enzymes such as GST, GGT, CAT, GPx, SOD, and GR, activating the Nrf2/HO‐1 pathway, elevating GSH content, and the reduction in MDA. The anti‐inflammatory effects of rutin are mediated by the inhibition of IL‐1β, IL‐6, TGF‐β1, COX‐2, iNOS, TLR4, and XO. Rutin exerted its antiapoptotic effects by inhibition of free radicals, caspase‐3/‐7/‐9, hsp70, HMGB1, and p53, and the elevation of the antiapoptotic protein Bcl‐2. Rutin has potential therapeutic effectiveness against several toxicants, and its beneficial effects are more than likely mediated by its antioxidant, anti‐inflammatory, and/or antiapoptotic property.

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Background and Objectives:Copper sulfate (CuSO4) is a toxic substance with a broad range of applications; however, the ingestion of high levels of it cause a wide range of complications in the liver tissue. According to previous studies, mitochondria are potential targets for CuSO4 toxicity. The present study aimed to examine the role of Nacetyl-cysteine as an antioxidant agent in the protection of mitochondria against toxicity induced by CuSO4. Methods:This study was performed on isolated liver mitochondria extracted from male Wistar rats (180-200 g) by multiple centrifuges and finally divided into 5 different groups. Group 1 was the control group, while group 2 received a single dose of 106 µM of CuSo4. The other groups were pretreated with different concentrations of N-acetylcysteine (1, 2, 5 mM) and exposed to 106 µM of CuSO4. Subsequently, MTT assay, lipid peroxidation, and GSH (reduced glutathione) were determined in each group. Finally, the collected data were analyzed using the one-way analysis of variance test. Results:The results of the present study revealed that significant changes in mitochondrial indexes such as mitochondrial complex Ⅱ function, mitochondrial glutathione reduction, and lipid peroxidation levels were evident in rat liver mitochondria exposed to CuSO4. On the other hand, it was found that pre-treatment with N-acetylcysteine efficiently inhibited CuSO4 toxicity. Conclusion:The results confirmed the protective effects of N-acetylcysteine against CuSO4 toxicity on rat liver mitochondria, which may be due to its ability to scavenge reactive oxygen species.