Zinc might prevent heat-induced hepatic injury by activating the Nrf2-antioxidant in mice.

Abstract

Zinc (Zn) is generally known to be an essential trace element with growth-promoting and antioxidant activities. The present study was performed to clarify the role of Zn in the livers of heat-treated mice. Eight-week-old male mice were divided into control (Con), heat treatment (HT) and heat treatment plus zinc groups (HT + Zn) and were fed diets containing 60, 60, or 300 mg/kg Zn (zinc sulfate), respectively. After 30 days of feeding on their respective diets, the control group was maintained at a controlled temperature (25 °C), whereas the HT and HT + Zn groups were exposed to an elevated ambient temperature (40-42 °C) for 2 h each day. After heat exposure for seven consecutive days, sera and liver tissues were collected. The mice in the HT group exhibited reduced liver weights and lower hepatosomatic indices. Histological findings revealed that the hepatocytes of the HT group were subjected to serious damage and exhibited irregular arrangements and nuclear pyknosis. Moreover, in the HT group, the hepatic malondialdehyde levels were significantly increased, while the serum alkaline phosphatase levels, hepatic copper/zinc-superoxide dismutase (CuZn-SOD) and glutathione peroxidase activities were significantly reduced compared to those of the control group. However, in the HT + Zn group, the histomorphology of the liver was restored, the serum aspartate aminotransferase (AST) level was significantly decreased, and the hepatic CuZn-SOD activity was significantly increased compared to the HT group. Furthermore, expressions of the hepatic Nrf2 protein and Nrf2, Keap1, and NQO1 genes in the HT + Zn group were not only higher than the HT group but also higher than the control group. Zn might alleviate heat-induced hepatic injury as revealed by restored histomorphology and AST level. Our results further suggest that Zn might exert its protective effects via the activation of the Nrf2-antioxidant pathway.