Rembacz Krzysztof P, Sawicka Ewa, Długosz Anna
Department of Toxicology, Wroclaw Medical University, Poland.
Acta Pol Pharm. 2012 Nov-Dec;69(6):1372-9.
This study investigated the role of 17beta-estradiol in chromium-generated oxidative stress in order to determine whether it has a detoxifying activity or increases the toxic effects of chromium compounds. Reduced glutathione (GSH) levels, membrane lipid peroxidation (levels of malondialdehyde -- MDA), glutathione peroxidase (GPx), and superoxide dismutase (SOD) activities were measured in blood. Isolated mitochondria were used to investigate the MDA levels and hydroxyl radical (OHradical) generation. The results showed a varying influence of estradiol on the chromium-induced oxidative stress. This paper demonstrated, that 17beta-estradiol showed a positive effect when erythrocytes were exposed to moderate concentrations of CrVI and increased the levels of erythrocytal GSH. Estradiol did not show any interactions with chromium on the antioxidative enzymes (SOD in erythrocytes and GPx in whole blood) activity measurements. Additionally, estradiol played a generally positive role in the chromium-induced lipid peroxidation in erythrocytes. Unexpectedly, the interaction of estradiol with chromium was found in human mitochondria, where estradiol increased the MDA levels induced by both forms of chromium. Estradiol also increased the OHradical generation triggered with CrVI. It appeared that estradiol acted protectively on lipid peroxidation caused by chromium in erythrocytes but gave an interaction with Cr in mitochondria, which partially correlated with hydroxyl radical formation in this organelle.
本研究调查了17β-雌二醇在铬产生的氧化应激中的作用,以确定它是否具有解毒活性或增加铬化合物的毒性作用。测定了血液中还原型谷胱甘肽(GSH)水平、膜脂质过氧化(丙二醛——MDA水平)、谷胱甘肽过氧化物酶(GPx)和超氧化物歧化酶(SOD)活性。使用分离的线粒体来研究MDA水平和羟自由基(OH˙)的产生。结果显示雌二醇对铬诱导的氧化应激有不同的影响。本文表明,当红细胞暴露于中等浓度的CrVI时,17β-雌二醇显示出积极作用,并增加了红细胞内GSH水平。在抗氧化酶(红细胞中的SOD和全血中的GPx)活性测量中,雌二醇与铬未显示出任何相互作用。此外,雌二醇在铬诱导的红细胞脂质过氧化中通常发挥积极作用。出乎意料的是,在人线粒体中发现了雌二醇与铬的相互作用,其中雌二醇增加了两种形式铬诱导的MDA水平。雌二醇还增加了由CrVI引发的OH˙产生。看来,雌二醇对红细胞中铬引起的脂质过氧化起保护作用,但与线粒体中的铬发生相互作用,这与该细胞器中的羟自由基形成部分相关。