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Review
. 2016 Sep;6(5):384-392.
doi: 10.1016/j.apsb.2016.07.014. Epub 2016 Aug 3.

Isoniazid metabolism and hepatotoxicity

Pengcheng Wang  1 , Komal Pradhan  1 , Xiao-Bo Zhong  2 , Xiaochao Ma  1
Affiliations
Review

Isoniazid metabolism and hepatotoxicity

Pengcheng Wang et al. Acta Pharm Sin B. 2016 Sep.

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.

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.

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Figures

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Graphical abstract
Fig. 1
Figure 1
A schematic representation of isoniazid (INH) metabolism and the enzymes involved in the metabolic pathways of INH. AcHz: acetylhydrazine; AcINH, acetylisoniazid; DiAcHz: diacetylhydrazine; GST: glutathione S-transferases; Hz: Hydrazine; INA: isonicotinic acid; MPO: myeloperoxidase; NAT2: N-acetyltransferase 2; P450: cytochrome P450; R.M.: reactive metabolite.
See this image and copyright information in PMC

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