Fulminant hepatic failure induced oxidative stress in nonsynaptic mitochondria of cerebral cortex in rats

• Published in: Neuroscience letters 2004-09, Vol.368 (1), p.15-20
• Main Authors: Reddy, P. Vijaya Bhaskar, Murthy, Ch.R.K., Reddanna, P.
• Format: Article
• Language: English
• Subjects: Animals; Biological and medical sciences; Brain Chemistry - physiology; Cerebral Cortex - metabolism; Fulminant hepatic failure; Fundamental and applied biological sciences. Psychology; Gastroenterology. Liver. Pancreas. Abdomen; Glutathione Reductase - metabolism; Hepatic Encephalopathy - chemically induced; Hepatic Encephalopathy - metabolism; Lipid Peroxidation - drug effects; Liver - enzymology; Liver - metabolism; Liver - pathology; Liver Failure, Acute - chemically induced; Liver Failure, Acute - metabolism; Liver Failure, Acute - pathology; Liver Function Tests; Liver. Biliary tract. Portal circulation. Exocrine pancreas; Male; Malondialdehyde - metabolism; Medical sciences; Mitochondria; Mitochondria - metabolism; Neurons - metabolism; Other diseases. Semiology; Oxidative stress; Oxidative Stress - physiology; Proteins - metabolism; Rats; Rats, Wistar; Sulfhydryl Compounds - metabolism; Superoxide Dismutase - metabolism; Synaptosomes - metabolism; Thioacetamide; Vertebrates: nervous system and sense organs
• ISSN: 0304-3940; 1872-7972
• DOI: 10.1016/j.neulet.2004.06.046

Fulminant hepatic failure (FHF) is a condition with sudden onset of necrosis of hepatocytes and degeneration of liver tissue without any established liver disease. FHF is associated with increased ammonia levels in blood and brain, which is supposed to be neurotoxic, ultimately leading to neuronal death. Evidences from previous studies suggest for mitochondrial dysfunctions under hyperammonemic conditions. In the present investigation, on thioacetamide-induced FHF rat models, studies were undertaken on cerebral nonsynaptic mitochondrial oxidative stress. The results of the present study reveal elevated lipid peroxidation along with reduced total thiol levels in the cerebral cortex mitochondria of experimental animals compared to saline treated control rats. In addition, the enzymatic activities of glutathione peroxidase and glutathione reductase were decreased, with an elevation in Mn-SOD activity. Overall, thioacetamide-induced FHF in rats enhanced the levels of lipid peroxidation coupled with impaired antioxidant defenses in the cerebral nonsynaptic mitochondria.