Heat Induced Oxidative Stress and Aberrations in Liver Function Leading to Hepatic Injury in Rats
Exposure to heat stress (HS) elicits systemic and cellular response in experimental animals and humans. The current study was undertaken to determine the effect of HS on liver microstructure and function in rats. A heat simulation chamber with ambient temperature (Ta) 45 ± 0.5 °C and relative humidity (RH) 30 ± 5 per cent was used to expose animals to HS. Rats were categorised as moderately heat stressed (MHS, Tc = 40 °C) and severely heat stressed (SHS, Tc = 42 °C) group. We observed that with rise in core temperature (Tc) alanine aminotransferase
(ALT), aspartate aminotransferase (AST) and alkaline phosphatase (ALP) levels were increased but glucose level was decreased in both plasma and liver tissue. Significantly elevated levels of reactive oxygen species (ROS) and nitric oxide (NO) were detected in liver of MHS and SHS animals. Additionally, glutathione disulfide and glutathione (GSSG and GSH) ratio was found to be increased with rise in Tc which suggested saturation in antioxidant capacity of tissue. Furthermore, levels of heat shock proteins (HSPs) and caspases were upregulated upon HS. Results of histological examination indicated extensive loss of cells in liver parenchyma leading to disorganisation of lobular structure. Thus, biochemical and histological studies in experimental animals demonstrates that HS may severely altered structural and biochemical functions of liver.
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