Oestradiol protects against the harmful effects of fluoride more by increasing thiol group levels than scavenging hydroxyl radicals

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Abstract

The aim of the study was to investigate the role of oestrogens in free radical detoxication upon exposure to fluoride. Interactions between xenobiotics and oestrogens need to be investigated, especially as many chemicals interact with the oestrogen receptor. It is still unknown whether free radical-generating xenobiotics can influence the antioxidative ability of oestradiol (E 2). In an in vitro examination of human placental mitochondria, thiobarbituric active reagent species (TBARS), hydroxyl radical ( •OH) generation and protein thiol (-SH) groups were detected. 17β-E2 was examined in physiological (0.15-0.73 nM) and experimental (1-10 μM) concentrations and sodium fluoride (NaF) in concentrations of 6-24 μM. E2 in all the concentrations significantly decreased lipid peroxidation measured as the TBARS level, in contrast to NaF, which increased lipid peroxidation. Lipid peroxidation induced by NaF was decreased by E2. The influence of E2 on •OH generation was not very significant and depended on the E2concentration. The main mechanism of E2 protection in NaF exposure appeared to be connected with the influence of E2on thiol group levels, not •OH scavenging ability. The E 2 in concentrations 0.44-0.73 nM and 1-10 μM significantly increased the levels of -SH groups, in contrast to NaF, which significantly decreased them. E2 at every concentration reversed the harmful effects of NaF on -SH group levels. No unfavourable interactions in the influence of E2 and NaF on TBARS production, •OH generation, or -SH group levels were observed. The results suggest that postmenopausal women could be more sensitive to NaF-initiated oxidative stress. © 2009 Nordic Pharmacological Society.

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APA

Dlugosz, A., Roszkowska, A., & Zimmer, M. (2009). Oestradiol protects against the harmful effects of fluoride more by increasing thiol group levels than scavenging hydroxyl radicals. Basic and Clinical Pharmacology and Toxicology, 105(6), 366–373. https://doi.org/10.1111/j.1742-7843.2009.00411.x

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