Advances in Clinical and Experimental Medicine

Adv Clin Exp Med
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ISSN 1899–5276 (print)
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Advances in Clinical and Experimental Medicine

2017, vol. 26, nr 2, March-April, p. 215–221

doi: 10.17219/acem/62217

Publication type: original article

Language: English

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Creative Commons BY-NC-ND 3.0 Open Access

The role of 17β-estradiol metabolites in chromium-induced oxidative stress

Ewa Sawicka1,A,B,C,D,E, Anna Długosz1,A,D,E,F

1 Department of Toxicology, Wroclaw Medical University, Poland

Abstract

Background. The increasing incidence of estrogen-dependent breast cancer and the presence in the environment of a large number of factors that interact with estrogen receptors have sparked interest in chemical influences on estrogen-dependent processes. In a previous work, the authors examined the interaction of estradiol with chromium. In the present article the importance of estradiol biotransformation in these interactions is investigated. There is no information in the available literature about the role of metabolites in exposure to chromium. It seems important because estradiol metabolites have various carcinogenic abilities and their formation during biotransformation could be increased or decreased by environmental enzyme inducers or inhibitors. The metabolites could play a detoxifying role or create a toxic synergism in free radical processes induced by chromium VI (CrVI).
Objectives. The aim of this study was to evaluate the influence of 2 17β-estradiol metabolites – 4-hydroxyestradiol (4-OHE2) and 16α-hydroxyestrone (16α-OHE1) – in conditions of oxidative stress caused by CrVI.
Material and Methods. Human blood, erythrocytes or mitochondria isolated from human placentas after natural deliveries were used in the experiments. The influence of CrVI, 4-OHE2 and 16-OHE1 on thiobarbituric acid reactive substances (TBARS), the hydroxyl radical (•OH), superoxide dismutase (SOD), glutathione peroxidase (GPx) and glutathione-S-transferase (GST), and the interactions of the metabolites exposed to chromium expressed by these factors were examined.
Results. 4-OHE2 reduced the level of TBARS induced by CrVI in mitochondria (p < 0.05) and in erythrocytes (p < 0.05), and increased SOD activity (p < 0.05). 16α-OHE1 increased the activity of GST in erythrocytes exposed to CrVI (p < 0.05).
Conclusion. The metabolites do not have toxic interactions with CrVI. On the contrary, they exhibited a protective effect. The mechanism of protection varied: 4-OHE2 decreased TBARS and increased SOD activity, while 16α-OHE1 increased GST activity.

Key words

oxidative stress, interactions, chromium VI, 4-hydroxyestradiol, 16α-hydroxyestrone

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