Chromium is widely present in the environment. Chromium toxicity is directly dependent on its valency. Chromium III (CrIII) is an essential factor of glucose metabolism as a constituent of the glucose tolerance factor (GTF) and chromium VI (CrVI) is considered carcinogenic in humans and is listed on the International Agency for Research on Cancer list of carcinogens. People exposed to chromium compounds express a number of disorders of variable background in some cases due to chromium-induced oxidative stress. Estrogens are involved in the anti- and pro- oxidative transformations as inducers or scavengers of reactive oxygen species.The aim of this study was to investigate the role of 17-β-estradiol in chromium-generated oxidative stress in order to determine whether it has a detoxifying activity or increases the toxic effects of chromium compounds.

Analyses described in this study were performed on an in vitro model of whole human blood, purified erythrocytes or mitochondria isolated from human placenta upon exposure to varying concentrations of CrIII, CrVI, and estradiol. 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 (˚OH) generation. The results show varying influence of estradiol on the chromium-induced oxidative stress.

We have shown previously (Dlugosz et al, 2012) that CrIII does not influence the levels of erythrocytal GSH, while CrVI at concentrations of 5 and 10 μg/mL  reduces the level of GSH in human red blood cells in vitro. In this work we noticed, that 17-β-estradiol shows a positive effect when erythrocytes are exposed to moderate concentrations CrVI and increases the levels of erythrocytal GSH. Estradiol does not show any interactions with chromium on the antioxidative enzymes (SOD in erythrocytes and GPx in whole blood) activity measurements. Additionally, we show that estradiol plays a positive role in the chromium-induced lipid peroxidation in erythrocytes, reducing the levels of MDA produced under exposition of erythrocytes to both forms of chromium. Unexpectedly, the interaction of estradiol with chromium can be seen on the MDA formation in human mitochondria, where estradiol increases MDA levels induced by both forms of chromium. Estradiol increased the ˚OH generation triggered with CrVI when compared to control mitochondria exposed to CrVI alone. It appears that estradiol acts protectively on lipid peroxidation caused by chromium in erythrocytes but gives an interaction with Cr in mitochondria, which partially correlates with hydroxyl radical formation in this organelle.

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