Oxidative stress, which is characterized by disruption of the oxidant/antioxidant balance, causes pathological processes, including toxicities induced by certain mycotoxins. The present study was designed to investigate the effects of resveratrol on sirtuin deacetylases (SIRT2 and SIRT3), nitric oxide (NO), reduced glutathione (GSH) and malondialdehyde (MDA) in fumonisin B1-induced hepatotoxicity. Regarding the experimental design, forty BALB/c mice were divided into four groups corresponding to the control, resveratrol (10 mg/kg, i.p), fumonisin B1 (2.25 mg/kg, i.p) and resveratrol + fumonisin B1 (10 mg/kg + 2.25 mg/kg) groups. At the end of the 14 day-treatment, expression levels of SIRT2 and SIRT3 protein in the serum and liver were revealed by western blotting and antioxidant/oxidant activity analysis. SIRT2 and SIRT3 expression levels in the liver were significantly decreased by fumonisin B1 in comparison to the control. However, resveratrol supplementation coupled with fumonisin B1 increased the expression levels of SIRT2 and SIRT3, in relation to the fumonisin B1 treatments alone, but did not exhibit significant differences from those of the control group. As substantial indicators of stress and damage, the 8-OH-2-deoxyguanosine, NO and MDA levels of the liver tissue were assayed, and were higher in the fumonisin B1-treated groups, in relation to the control. As expected, resveratrol treatment significantly reduced the levels of NO and MDA in comparison to the fumonisin B1 treatments alone. Also, resveratrol attenuated the liver 8-OH-2- deoxyguanosine levels in the resveratrol + fumonisin B1 group. In conclusion, the findings revealed that resveratrol might possess protective effects against fumonisin-induced hepatotoxicity through modulation of the expression of sirtuin proteins, and by protecting the cell from oxidative/nitrosative stress.

The aim of this study was to investigate the effects of resveratrol against fumonisin B1 (FB1)-induced liver toxicity, as, to the best of our knowledge, these effects have not been investigated yet, even though the toxic effects and mechanisms of FB1 and the antioxidative effects of resveratrol are well known. 40 BALB/c mice were divided into control, FB1, resveratrol, and FB1+resveratrol groups. Control received saline for 14 days. The FB1 group received 2.25 mg/kg FB1 every other day for 14 days. The resveratrol group received 10 mg/kg resveratrol for 14 days. The FB1+resveratrol group received 2.25 mg/kg FB1 every other day and 10 mg/kg resveratrol every day for 14 days. All administrations were peritoneal. Alanine aminotransferase (ALT), aspartate aminotransferase (AST), total sialic acid (TSA) levels were analysed in serum samples, while total antioxidant status (TAS) and total oxidant status (TOS) were measured in the liver. Additionally, the liver tissue was examined for histopathological changes. AST, ALT, and TSA were significantly higher in the FB1 group than control. Resveratrol countered FB1 effects for all parameters, including TOS and TAS. Liver histology showed FB1-induced hyperaemia, infiltrations, and megalokaryosis in some hepatocytes. No pathological findings were detected in the control, resveratrol, or FB1+resveratrol group. Our findings confirm resveratrol’s protective effect against liver damage and oxidative stress caused by FB1. In addition, they suggest that increased serum TSA levels can be used as a biomarker of FB1-induced hepatotoxicity.