Role of Metabolism In 1-Bromopropane-Induced Hepatotoxicity in Mice
- Role of Metabolism In 1-Bromopropane-Induced Hepatotoxicity in Mice
- 이상규; 강미정; 전태원; 하현우; 유진우; 고규섭; 강원구; 정혜광[정혜광]; 류원석; 정태천
- FEMALE BALB/C MICE; CENTRAL-NERVOUS-SYSTEM; GLUTATHIONE CONJUGATION; BIOCHEMICAL-CHANGES; MERCAPTURIC ACIDS; ICR MICE; RATS; IMMUNOTOXICITY; ACTIVATION; INDUCTION
- Issue Date
- TAYLOR & FRANCIS INC
- JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH-PART A-CURRENT ISSUES, v.73, no.21-22, pp.1431 - 1440
- A possible role of metabolism in 1-bromopropane (1-BP)-induced hepatotoxicity was investigated in male ICR mice. The depletion of glutathione (GSH) by formation of GSH conjugates was associated with increased hepatotoxicity in 1-BP-treated mice. The formation of S-propyl and 2-hydroxypropyl GSH conjugates were identified in the liver following 1-BP treatment. In addition, the formation of reactive metabolites of 1-BP by certain cytochrome P-450 (CYP) may be involved in 1-BP-induced hepatotoxicity. The decreased content of hepatic GSH produced by 1-BP was associated not only with increased activities of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) but also with elevated levels of hepatic thiobarbituric acid-reactive substance (TBARS) in mice where metabolic enzymes were induced by pretreatment with phenobarbital. In addition, the hepatotoxicity induced by 1-BP was prevented by pretreatment with SKF-525A. Taken together, the formation of reactive metabolites by CYP and depletion of GSH may play important roles in hepatotoxicity induced by 1-BP.
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