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六价铬诱导大鼠子宫细胞凋亡:氧化应激的作用

Hexavalent Chromium-Induced Apoptosis in Rat Uterus: Involvement of Oxidative Stress.

作者信息

Marouani Neila, Tebourbi Olfa, Mokni Moncef, Yacoubi Mohamed Tahar, Sakly Mohsen, Benkhalifa Moncef, Rhouma Khémais Ben

机构信息

a Laboratoire de Physiologie Intégrée, Faculté des Sciences de Bizerte , Zarzouna , Tunisia.

出版信息

Arch Environ Occup Health. 2015;70(4):189-95. doi: 10.1080/19338244.2013.828673.

Abstract

The present study is designed to test the hypothesis that oxidative stress mediates hexavalent chromium (VI)-induced apoptosis in uterus. Female Wistar rats received an intraperitoneal (i.p.) injection of potassium dichromate at doses of 1 and 2 mg/kg. Superoxide anion production was assessed by determination of the reduction of cytochrome c and iodonitrotetrazolium (INT), lipid peroxidation (LPO), metallothioneins (MTs), and catalase (CAT) activity. The expression of Bax and Bcl-2 proteins was investigated. After 15 days of treatment, an increase of LPO and MT levels occurred, whereas CAT activity decreased. Intense apoptosis was observed in endometriotic stromal cells of Cr-exposed rats. Bax protein expression was induced in endometriotic stromal cells with 1 mg of Cr(VI)/kg, and in stromal and epithelial cells at the higher dose. These results clearly suggest that Cr(VI) subacute treatment causes oxidative stress in rat uterus, leading to endometriotic stromal cells apoptosis.

摘要

本研究旨在验证氧化应激介导六价铬(VI)诱导子宫细胞凋亡的假说。雌性Wistar大鼠腹腔注射剂量为1和2mg/kg的重铬酸钾。通过测定细胞色素c和碘硝基四氮唑(INT)的还原率、脂质过氧化(LPO)、金属硫蛋白(MTs)和过氧化氢酶(CAT)活性来评估超氧阴离子的产生。研究了Bax和Bcl-2蛋白的表达。治疗15天后,LPO和MT水平升高,而CAT活性降低。在铬暴露大鼠的子宫内膜间质细胞中观察到强烈的细胞凋亡。1mg Cr(VI)/kg剂量时,子宫内膜间质细胞中Bax蛋白表达被诱导,高剂量时在间质细胞和上皮细胞中也被诱导。这些结果清楚地表明,六价铬亚急性处理会导致大鼠子宫氧化应激,进而导致子宫内膜间质细胞凋亡。

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