Resveratrol Attenuates Aflatoxin B-Induced ROS Formation and Increase of mA RNA Methylation.

Aflatoxin B (AFB) is one of the most dangerous mycotoxins in both humans and animals. Regulation of resveratrol is essential for the inhibition of AFB-induced oxidative stress and liver injury. Whether N-methyladenosine (mA) mRNA methylation participates in the crosstalk between resveratrol and AFB is unclear. The objective of this study was to investigate the effects of AFB and resveratrol in mA RNA methylation and their crosstalk in the regulation of hepatic function in mice. Thirty-two C57BL/6J male mice were randomly assigned to a CON (basal diet), RES (basal diet + 500 mg/kg resveratrol), AFB (basal diet + 600 μg/kg aflatoxin B), and ARE (basal diet + 500 mg/kg resveratrol and 600 μg/kg aflatoxin B) group for 4 weeks of feeding ( = 8/group). Briefly, redox status, apoptosis, and mA modification in the liver were assessed. Compared to the CON group, the AFB group showed increased activities of serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT), prevalent vacuolization and cell edema, abnormal redox status, imbalance apoptosis, and especially, the higher expression of cleaved-caspase-3 protein. On the contrary, resveratrol ameliorated adverse hepatic function, via increasing hepatic antioxidative capacity and inhibiting the expression of cleaved-caspase-3 protein. Importantly, we noted that reactive oxygen species (ROS) content could be responsible for the alterations of mA modification. Compared to the CON group, the AFB group elevated the ROS accumulation, which led to the augment in mA modification, whereas dietary resveratrol supplementation decreased ROS, followed by the reduction of mA levels. In conclusion, our findings indicated that resveratrol decreased AFB-induced ROS accumulation, consequently contributing to the alterations of mA modification, and eventually impacting on the hepatic function.