期刊
DRUG METABOLISM REVIEWS
卷 40, 期 3, 页码 465-477出版社
TAYLOR & FRANCIS LTD
DOI: 10.1080/03602530802186587
关键词
glutathione; glutamate-cysteine ligase; transgenic; gene-targeting; acetaminophen; liver injury; mice
资金
- NIEHS NIH HHS [T32ES07032, R01ES10849, U19ES11378, P42ES04696, P30ES07033] Funding Source: Medline
- NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES [P42ES004696, P30ES007033, R01ES011378, R01ES010849, T32ES007032] Funding Source: NIH RePORTER
Glutathione (GSH) is an important antioxidant and cofactor for glutathione S-transferase conjugation. GSH synthesis is catalyzed by glutamate cysteine ligase (GCL), composed of catalytic (GCLC) and modifier (GCLM) subunits. Transgenic mice that conditionally over express GCL subunits are protected from acetaminophen induced liver injury. Gclm null mice exhibit low GSH levels and enhanced sensitivity to acetaminophen. When Gclm expression and GCL activity are restored in Gclm conditional transgenic X Gclm null mice, they become resistant to APAP-induced liver damage. These animal models are a valuable resource for investigating the role of GSH synthesis in modulating oxidative damage and drug-induced hepatotoxicity.
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