Zitting A, Savolainen H, Nickels J
Toxicol Lett. 1981 Nov;9(3):237-46. doi: 10.1016/0378-4274(81)90156-9.
Intraperitoneal injection (50 mg/kg) of 2-nitropropane (2-NP) induced lipid accumulation, centrilobular necrosis, degranulation of rough endoplasmic reticulum, proliferation of smooth endoplasmic reticulum and mitochondrial abnormalities in rat liver 24 h after exposure. These pathological changes were accompanied by elevated serum alanine aminotransferase (ALAT) levels. Hepatic glutathione content increased rapidly in exposed rats. 2-NP depressed markedly hepatic cytochrome P-450 and microsomal monooxygenase activity while the enzyme, epoxide hydratase, UDP-glucuronosyltransferase and cytosolic glutathione peroxidase were enhanced. 2-NP caused an increase of acetylcholine esterase activity in the brain. This effect was also detected in synaptosomes isolated from exposed rats. The results suggest peroxidative damage in the cells.
腹腔注射（50毫克/千克）2-硝基丙烷（2-NP）可在大鼠接触24小时后诱导肝脏脂质蓄积、小叶中心坏死、粗面内质网脱颗粒、滑面内质网增生以及线粒体异常。这些病理变化伴随着血清丙氨酸转氨酶（ALAT）水平升高。暴露大鼠肝脏中的谷胱甘肽含量迅速增加。2-NP显著降低肝脏细胞色素P-450和微粒体单加氧酶活性，而环氧化物水解酶、UDP-葡萄糖醛酸转移酶和胞质谷胱甘肽过氧化物酶活性增强。2-NP导致大脑中乙酰胆碱酯酶活性增加。从暴露大鼠分离的突触体中也检测到这种效应。结果提示细胞存在过氧化损伤。
