Experimental observation of mitochondrial oxidative damage of liver cells induced by isonicotinic acid hydrazide.

The aim of the present study was to investigate the oxidative damage of liver mitochondria as an adverse effect of the anti-tuberculosis drug isonicotinic acid hydrazide (INH). The human hepatoblastoma cell line (HepG2) was exposed to INH at concentrations of 0, 1, 2 or 4 mg/ml for 24, 48, 72 or 96 h, and the levels of malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and 8-hydroxy-2-deoxyguanosine (8-OHdG) in mitochondria were detected. Changes in the mitochondrial ultrastructure were observed by electron microscopy. Along with the increase of incubation time and dose of INH, activities of mitochondrial SOD and GSH-Px decreased, MDA and 8-OHdG content increased, and the mitochondrial ultrastructure displayed varying degrees of pathological changes. In conclusion, INH was found to cause liver cell injury by inducing mitochondrial DNA damage.