Hepatoprotective Effect of Liv. 100, a Polyherbal Formulation, on Mitochondrial Enzymes in Anti-Tubercular Drug-Induced Liver Damage in Rats.

Abstract

We studied the anti-hepatotoxic potential of Liv.100, a herbal formulation, on anti-tubercular (anti-TB) drugs [isoniazid (INH), rifampicin (RMP), and pyrazinamide (PZA)]-induced mitochondrial damage in rat liver. Liv.100 (400mg/kg body wt./day, orally) was administered simultaneously with anti-TB drugs for 6 weeks. Activities of TCA cycle enzymes (succinate dehydrogenase, isocitrate dehydrogenase, malate dehydrogenase, and α-ketoglutarate dehydrogenase) and respiratory marker enzymes (cytochrome c oxidase, NADH dehydrogenase) and levels of mitochondrial lipid peroxidation in liver were determined. Activities of TCA cycle enzymes and respiratory marker enzymes were significantly lower upon anti-TB drug treatment than those of normal controls. Mitochondrial lipid peroxidation was found to be increased when compared with the normal control value. This indicates impaired function of hepatic mitochondria in anti-TB drug-induced hepatocellular damage. In our present study, Liv.100 co-administration significantly reduced the anti-TB drug-induced alterations in the level of lipid peroxide and activities of TCA cycle enzymes and respiratory marker enzymes in liver mitochondria. The mechanism of action of Liv.100 is probably due to its antioxidant nature against anti-TB drug-induced lipid peroxidation, which is mainly responsible for the inhibition of these enzyme activities.