Advanced medical services and treatments are available for treating Tuberculosis. Related
prevalence has increased in recent times. Unfortunately, the continuous consumption of related drugs is
also known for inducing hepatotoxicity which is a critical condition and cannot be overlooked. The
present review article has focused on the pathways causing these toxicities and also the role of enzyme
CYP2E1, hepatic glutathione, Nrf2-ARE signaling pathway, and Membrane Permeability Transition as
possible targets which may help in preventing the hepatotoxicity induced by the drugs used in the
treatment of tuberculosis.
Keywords: Isoniazid, rifampicin, hepatotoxicity, oxidative stress, anti-tuberculosis drugs, pharmacology.
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