Heat stress-induced hepatotoxicity and its prevention by resveratrol in rats

Abstract

The high ambient temperature beyond the range of comfort zone or thermoneutral zone causes environmental heat stress (HST). It causes serious physiological dysfunction that may result in heat-related diseases and even death. The underlying mechanism in the pathogenesis of hepatic dysfunction following hyperthermic challenge and the possible involvement of oxidative stress to induce oxidative deterioration of liver functions in adult rats are investigated in this study. Cellular damage was assessed in terms of serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities and histology of liver. The effect of hyperthermia in altering the oxidative stress was evaluated on the basis of its influence on hepatic lipid peroxidation and antioxidant status—superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) activity. The current study demonstrated that HST is associated with a complex set of integrated alterations in liver, time-dependent rise in oxidative stress followed by distinct pattern of liver injury in animals. Heat-induced hepatotoxicity was assessed by increased lipid peroxidation, depletion of antioxidant enzyme activities such as SOD, CAT, GPx and tissue damages revealed by hepatic vacuolization, and widespread necrosis. The study also revealed that pretreatment with resveratrol resulted in normalizing these parameters appreciably, emphasizing the therapeutic potentials of this polyphenol. Taken together, the results suggest that an increase in free radical formation relative to loss of the antioxidant defense system during heat stress may render liver more susceptible to oxidative damage, leading to their functional inactivation. However, resveratrol supplementation can be an effective antidote in the treatment of HST-induced malfunction.

Keywords::

• Heat stress
• resveratrol
• antioxidant enzymes
• lipid peroxidation
• liver

Acknowledgement

The author is grateful to Dr. Syed N. Kabir, Scientist, Cell Biology and Physiology Division, Indian Institute of Chemical Biology (IICB), Kolkata for the facilities provided to conduct the work and also thankful to Dr. Rituparna Ghosh, Department of Physiology, Bhairab Ganguly College, Kolkata, for technical assistance.

Declaration of interest

The financial assistance from University Grants Commission (Eastern Regional Office), Kolkata is gratefully acknowledged. The author reports no conflict of interest. The author alone is responsible for the content and writing of the paper.