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2-硝基丙烷对大鼠肝脏和大脑的急性影响。

Acute effects of 2-nitropropane on rat liver and brain.

作者信息

Zitting A, Savolainen H, Nickels J

出版信息

Toxicol Lett. 1981 Nov;9(3):237-46. doi: 10.1016/0378-4274(81)90156-9.

Abstract

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.

摘要

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。

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