Fulminant hepatic failure (FHF) is a condition with a sudden onset of
necrosis followed by degeneration of hepatocytes, without any previously established
liver disease, generally occurring within hours or days. FHF is associated with a wide spectrum of neuropsychiatric alterations ranging from stupor to
coma, culminating in death. In the present study FHF was induced in rats by the administration of
thioacetamide (TAA). Oxidative stress is thought to play a prominent role in the pathophysiology of cerebral changes during FHF leading to the assumption that
antioxidants might offer protection. Hence, in the present study the protective effect of
C-Phycocyanin (C-PC), a natural
antioxidant, was evaluated on TAA-induced tissue damage.
C-Phycocyanin was administered intraperitoneally twice at 24 h interval (50 mg/kg
body weight) along with the hepatotoxin TAA (300 mg/kg
body weight). The animals were sacrificed 18 h after the second injection of TAA treatment and various biochemical parameters were analysed in liver, serum and brain tissues. These studies revealed significant prevention of TAA-induced liver damage by C-PC, as evidenced by a) increase in survival rate; b) the prevention of leakage of liver
enzymes (AAT and AST) and
ammonia into serum; c) increase in prothrombin time and d) liver histopathology. Ultrastructural studies of astrocytes of different regions of brain clearly showed a decrease in
edema after C-PC treatment. TAA-induced histopathological lesions in different regions of the brain namely cerebral cortex, cerebellum and pons medulla were significantly reduced by the co-administration of C-PC with TAA. Further C-PC treatment resulted in a) decrease in the levels of
tryptophan and markers of lipid peroxidation and b) elevation in the activity levels of
catalase,
glutathione peroxidase in different regions of brain. These studies reveal the potential of C-PC in ameliorating TAA-induced
hepatic encephalopathy by improving
antioxidant defenses.