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| Research article summary (published 29 Sep 2009): |
Selenium increases expression of HSP70 and antioxidant enzymes to lessen oxidative damage in Fincoal-type fluorosis.
Full Abstract
Fincoal type fluorosis has only been reported from China, but its pathogenesis is unclear. Many people believe that fluorosis is associated with oxidative stress. Oxidative stress can be reduced at higher selenium (Se) level. Heat shock protein (HSP70) is the most conserved and induced against different stressors. The aim of this study is to detect the expression of HSP70 in fluorosis patients and explore the role of Se in fluorosis protection. The subjects were divided into four groups: "High Se + F group" (n = 50), "High F group" (n = 50), "High Se group" (n = 20) and "Control group" (n = 46). Expression of HSP70 was evaluated by Western blotting and real-time PCR techniques. The concentration of fluoride, content of Se in hair, activity of antioxidant enzymes (GSH-Px, SOD, CAT) and content of malondialdehyde (MDA) were determined. The relative amount of HSP70 gene transcription was significantly higher in "High Se + F group" than the other groups. The same results were found for expression of HSP70 protein to beta-actin ratio. There was a significant difference between "High Se + F group" and "High F group" regarding MDA content and glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) and catalase (CAT) activity. These results suggest that oxidative stress plays an important role in the pathogenesis of the Fincoal type fluorosis and it can be reduced at higher Se level.
Author information
Author/s: Chen, Qun (Q); Wang, Zhilun (Z); Xiong, Yongmin (Y); Xue, Wanli (W); Kao, Xibin (X); Gao, Yan (Y); Muhammad, Nawaz (N); Song, Daiqin (D);
Journal and publication information
Publication Type: Letter; Research Support, Non-U.S. Gov't
Journal: The Journal of toxicological sciences (J Toxicol Sci), published in Japan. (Language: eng)
Reference: 2009-Oct; vol 34 (issue 4) : pp 399-405
Dates: Created 2009/08/04; Completed 2009/11/02;
PMID: 19652462, status: MEDLINE (last retrieval date: 11/2/2009, IMS Date: )
Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.
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