PurposeTo investigate the effect of hepatocyte toxicity induced by isoniazid with oxidative stress in vitro. Try to set up a new hepatotoxicity model in the oxidative stress state and explore the injury mechanisms in drug-induced hepatotoxicity.MethodsThe level of serum alanine transaminase(ALT) , aspartate aminotransferase(AST), lactate dehydrogenase(LDH),cell viability, changes in morphology of hepatocyte were investigated in glucose+glucose oxidase group, isoniazid group, isoniazid + glucose+glucose oxidase group ,isoniazid + glucose + glucose oxidase +reduced glutathione hormone group and normal control group.To investigate the effect of hepatocyte toxicity induced by isoniazid with oxidative stress in vitro.ResultsCompared with isoniazid group,the activities of serum ALT, AST and LDH (p<0.05)were markedly increased in the isoniazid + glucose + glucose oxidase group and the viabilities of human normal liver L-02 cells significantly decreased,(p<0.05). Compared with isoniazid + glucose + glucose oxidase group , the activities of serum ALT, AST and LDH(p<0.05) were markedly reduced in the isoniazid + glucose + glucose oxidase +reduced glutathione group and the viabilities of human normal liver L-02 cells significantly increased,(p<0.05).Conclusion0.5mmol/L Glucose and 0.025U/ml glucose oxidase can lead to human normal liver L-02 cells in the non-toxicity oxidative stress state. Odative stress exacerbates isoniazid induced hepatocyte toxicity in human normal liver L-02 cells in vitro.Reduced glutathione has a obviously protective effects on human normal liver L-02 cells injured by isoniazid in which oxidative stress state. |