Isoniazid metabolism and hepatotoxicity.
- Author:
Pengcheng WANG
1
;
Komal PRADHAN
1
;
Xiao-Bo ZHONG
2
;
Xiaochao MA
1
Author Information
1. Center for Pharmacogenetics, Department of Pharmaceutical Sciences, School of Pharmacy, University of Pittsburgh, Pittsburgh, PA 15261, USA.
2. Department of Pharmaceutical Sciences, School of Pharmacy, University of Connecticut, Storrs, CT 06269, USA.
- Publication Type:Review
- 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
- From:
Acta Pharmaceutica Sinica B
2016;6(5):384-392
- CountryChina
- 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.
