Isoniazid (INH) is highly effective for the management of tuberculosis. However, it can cause liver injury and even liver failure. INH metabolism has been thought to be associated with INH-induced liver injury. This review summarized the metabolic pathways of INH and discussed their associations with INH-induced liver injury.
Keywords: ALP, alkaline phosphatase; ALT, alanine aminotransferase; AcHz, acetylhydrazine; AcINH, acetylisoniazid; Amidase; Anti-tuberculosis; DiAcHz, diacetylhydrazine; GSH, glutathione; GST, glutathione S-transferase; Hepatotoxicity; Hz, hydrazine; INA, isonicotinic acid; INH, isoniazid; Isoniazid; MPO, myeloperoxidase; Metabolism; N-Acetyltransferase 2; NAD+, nicotinamide adenine dinucleotide; NAT, N-acetyltransferase; P450, cytochrome P450; R.M., reactive metabolite; TB, tuberculosis.