Chronic Liver Failure Induces Oxidative Stress and Mitochondrial Dysfunction in Rat Hippocampus

Abstract

193 DOI: 10.37398/JSR.2022.660121 Abstract: Brain functions are intricately linked to the proper functioning of the liver such that compromised liver function led buildup of neurotoxins, like ammonia, in the cerebral circulation is argued to derange brain functions in many ways. The neuronal damage during chronic liver failure (CLF) seems to be associated with oxidative stress and bioenergetic derangements. We have attempted to examine the level of oxidative stress markers and mitochondrial dysfunction in the hippocampus of the rats with CLF induced by administration of 100 mg/Kg bw thioacetamide (TAA).; ip. As compared to the control group rats, the CLF rats showed declined levels of the key antioxidant enzymes like superoxide dismutase, glutathione peroxidase and small molecule antioxidant glutathione in their hippocampus. This was consistent with the enhanced level of lipid peroxidation and protein carbonyl content. The significantly declined level of cellular ATP, the enhanced mitochondrial ROS level and release of mitochondrial cytochrome c in the hippocampus further suggested deranged mitochondrial function in this brain region of the CLF rats. The findings suggest imposition of oxidative stress and mitochondrial dysfunction in the hippocampus due to CLF in rats.