Katoh T, Higashi K, Inoue N, Tanaka I
Department of Environmental Toxicology, School of Medicine, University of Occupational and Environmental Health, Kitakyushu, Japan.
Res Commun Chem Pathol Pharmacol. 1988 Aug;61(2):281-4.
The chronic effects of ethylene oxide (EO) on hepatic metabolism were investigated. Both reduced and oxidized forms of glutathione in liver were not changed during chronic exposure to EO for 13 weeks. On the other hand, increased levels of malondialdehyde were detected at 6 weeks and at the end of exposure periods, as compared with those of control livers. The activity of glutathione reductase was decreased at 6 and 13 weeks and therefore in inverse proportion to the lipid peroxide, although the reduced form of glutathione did not decrease probably due to the increase of de novo synthesis. These results indicate that EO treatment enhances lipid peroxidation and also affects glutathione redox cycle, but glutathione did not play a causative role in the induction of lipid peroxidation under the present conditions.
研究了环氧乙烷(EO)对肝脏代谢的慢性影响。在长达13周的慢性EO暴露期间,肝脏中还原型和氧化型谷胱甘肽均未发生变化。另一方面,与对照肝脏相比,在暴露6周时以及暴露期末检测到丙二醛水平升高。谷胱甘肽还原酶的活性在6周和13周时降低,因此与脂质过氧化物呈反比,尽管还原型谷胱甘肽可能由于从头合成增加而未减少。这些结果表明,EO处理可增强脂质过氧化作用并影响谷胱甘肽氧化还原循环,但在当前条件下,谷胱甘肽在脂质过氧化诱导中未起因果作用。