Acta Pharmaceutica Sinica B 2016;6(5):384-392
Isoniazid metabolism and hepatotoxicity.
Pengcheng WANG 1 ; Komal PRADHAN 1 ; Xiao-Bo ZHONG 2 ; Xiaochao MA 1
Affiliations
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
Country
China
Language
English
Abstract
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.
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