Fujita M, Sano M, Yoshino K, Tomita I
Laboratory of Health Science, School of Pharmaceutical Sciences, University of Shizuoka, Japan.
Biochem Mol Biol Int. 1994 Mar;32(3):429-34.
The relative contribution of the aldehyde dehydrogenase (EC 1.2.1.3, ALDH) and glutathione (GSH) conjugate system to the degradation of (E)-4-hydroxy-2-nonenal (4HN), a toxic breakdown product arising from lipid peroxidation, was investigated in rat liver. Significant increases in the contents of 4HN and hexanal (HA) and a decrease of ALDH but not alcohol dehydrogenase (EC 1.1.1.2, ADH) activity were recognized in rat liver following administration of carbon tetrachloride (3 ml/kg, p.o.). Hepatic ALDH activity was correlated with HA production (r = -0.82, P < 0.01) but not with 4HN. When lipid peroxidation was induced by t-butyl hydroperoxide, the ratio of HA to 4HN production in the liver of rats pretreated with the ALDH inhibitor, cyanamide (100 mg/kg, i.p.) was higher than that in controls, whereas the ratio was lower in the liver of rats pretreated with the glutathione-depleting agent, phorone (250 mg/kg, i.p.). These results suggest that 4HN in rat liver is metabolized by the GSH-conjugate system in preference to degradation by ALDH.
在大鼠肝脏中，研究了醛脱氢酶（EC 1.2.1.3，ALDH）和谷胱甘肽（GSH）结合系统对（E）-4-羟基-2-壬烯醛（4HN）降解的相对贡献，4HN是脂质过氧化产生的一种有毒分解产物。给予四氯化碳（3 ml/kg，口服）后，大鼠肝脏中4HN和己醛（HA）含量显著增加，ALDH活性降低，但乙醇脱氢酶（EC 1.1.1.2，ADH）活性未降低。肝脏ALDH活性与HA生成相关（r = -0.82，P < 0.01），但与4HN无关。当用叔丁基过氧化氢诱导脂质过氧化时，用ALDH抑制剂氰胺（100 mg/kg，腹腔注射）预处理的大鼠肝脏中HA与4HN生成的比率高于对照组，而用谷胱甘肽耗竭剂佛尔酮（250 mg/kg，腹腔注射）预处理的大鼠肝脏中该比率较低。这些结果表明，大鼠肝脏中的4HN优先通过GSH结合系统代谢，而不是通过ALDH降解。
