Isoniazid is one of the most commonly used drugs to treat tuberculosis. Its administration is associated with a high incidence of hepatotoxicity. The aim of this study was to establish the protective effects of taurine against cytotoxicity induced by isoniazid and its suspected toxic metabolite hydrazine in isolated rat hepatocytes by measuring reactive oxygen species (ROS) formation, lipid peroxidation, mitochondrial depolarisation, reduced glutathione (GSH), and oxidised glutathione (GSSG). Isoniazid caused no significant ROS formation in normal hepatocytes, but in glutathione-depleted cells it was considerable. Hydrazine caused ROS formation and lipid peroxidation in both intact and glutathione-depleted cells. Both isoniazid and hydrazine caused mitochondrial membrane depolarisation. Hydrazine lowered cellular GSH reserve and increased GSSG. Taurine (200 μmol L ) and N-acetylcysteine (200 μmol L-1) effectively countered the toxic effects of isoniazid and/or hydrazine by decreasing ROS formation, lipid peroxidation, and mitochondrial damage. Taurine prevented depletion of GSH and lowered GSSG levels in hydrazine-treated cells. This study suggests that the protective effects of taurine against isoniazid and its intermediary metabolite hydrazine cytotoxicity in rat hepatocytes could be attributed to antioxidative action. Izoniazid je jedan od najčešćih lijekova za tuberkulozu, ali se njegova primjena povezuje s veoma učestalom hepatotoksičnosti. Cilj je ovog istraživanja bio ocijeniti djelotvornost taurina u zaštiti izoliranih hepatocita štakora od citotoksičnosti izazvane izoniazidom i njegovim toksičnim metabolitom hidrazinom. U tu smo svrhu utvrdili razine reaktivnih kisikovih spojeva (ROS), lipidnu peroksidaciju, depolarizaciju mitohondrija, reducirani glutation (GSH) te oksidirani glutation (GSSG). Izoniazid nije doveo do značajnoga nastanka ROS-a u normalnih hepatocita, ali je zato bio značajan u stanica osiromašenih glutationom. I izoniazid i hidrazine doveli su do depolarizacije membrane mitohondrija. Hidrazin je smanjio staničnu rezervu GSH i povećao razinu GSSG. Taurin (200 μmol L-1) i N-acetilcistein (200 μmol L ) uspješno su zaštitili od toksičnoga djelovanja izoniazida i/ili hidrazina, smanjivši nastanak ROS-a, lipidnu peroksidaciju i oštećenje mitohondrija. Taurin je spriječio potpuni gubitak GSH-a te snizio razine GSSG-a u stanica tretiranih hidrazinom. Rezultati našeg istraživanje upućuju na to da se zaštitno djelovanje taurina od stanične toksičnosti izoniazida i hidrazina može pripisati njegovu andioksidacijskome djelovanju.