Zitting A, Nickels J, Savolainen H
Toxicol Lett. 1982 Oct;13(3-4):189-94. doi: 10.1016/0378-4274(82)90211-9.
Male 3-month-old Wistar rats dosed i.p. with 200 mg/kg of nitromethane or -ethane showed increased acid proteinase activity in the brain 4 h after the injection. The change was accompanied by a marginal increase in the cerebral glutathione concentration. Nitroethane caused enhanced epoxide hydrolase and UDP-glucuronosyltransferase activity in the hepatic microsomal fraction up to 48 h while 7-ethoxycoumarin o-deethylase decreased. These biochemical changes were accompanied by proliferation of smooth endoplasmic reticulum and degranulation and disorganization of the rough endoplasmic reticulum of the nitroethane-exposed liver cells. The hepatic effects of nitromethane were restricted to decreased cytochrome c reductase activity with proliferation of smooth endoplasmic reticulum. The results point at limited peroxidative damage possibly involving reduction of the nitrogroup.
对3个月大的雄性Wistar大鼠腹腔注射200mg/kg的硝基甲烷或硝基乙烷后，在注射后4小时，其大脑中的酸性蛋白酶活性增加。这种变化伴随着大脑谷胱甘肽浓度的轻微增加。硝基乙烷使肝微粒体部分的环氧化物水解酶和UDP-葡萄糖醛酸基转移酶活性增强，持续至48小时，而7-乙氧基香豆素O-脱乙基酶活性降低。这些生化变化伴随着暴露于硝基乙烷的肝细胞的滑面内质网增殖以及粗面内质网的脱颗粒和紊乱。硝基甲烷对肝脏的影响仅限于细胞色素c还原酶活性降低以及滑面内质网增殖。结果表明可能涉及硝基还原的有限过氧化损伤。
