Abstract

Hepatotoxicity is an injury to liver that is associated with impaired liver function caused by exposureto a drug or another non-infectious agent. Iatrogenic hepatotoxicity and their end stage liver cirrhosisare in the sphere of interest of scientists and clinicians. Long term use, especially in high dose, of tetracyclineantibiotic may cause adipose liver dystrophy with accumulation of reactive oxygen species and lipidperoxidation due to mainly mitochondrial dysfunctions. Continuous efforts were done to understand therole of oxidative stress in the pathophysiology of these inflammatory liver diseases. The well documemedscavenging activity (an antioxidant effect) of herbal agents namely; Silymarin, Liv-52 and DiphenylDimethyl Bicarboxylate ( DDB) may explain the protection afforded by these substances against hepatotoxicagents; The efficacy and the mechanism of these hepatoprotective agents were judged in this study.Oral administration of tetracycline (500 mg/kg orally) for 5 days in rats produced significant increase inboth serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels as a markers ofliver parenchymal toxicity and produced significant increase of liver malondialdhyde (MDA) level andsignificant depletion of both superoxide dismutase (SOD) activity and glutathione (GSH) concentration inliver homogenate compared with normal rats. Histopathologically, tetracycline treatment in the aboveregimen produced a picture of microvesicular steatosis. Co-administration of tetracycline with either silymarin,Liv-52 or DDB orally for 5 days produced significant decrease in serum ALT and AST and producedsignificant decrease in MDA and significant increase in both SOD activity and GSH content of liverhomogenate compared with tetracycline alone treated group. These herbal agents produced variabledegrees of improvement in histopathological changes induced by tetracycline treatment.

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