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Article type: Research Article
Authors: Chanoine, Jean-Pierre | Compagnone, Nathalie A. | Wong, Alfred C.K. | Mellon, Synthia H.
Affiliations: Department of Pediatrics, Endocrine and Diabetes Unit, University of British Columbia, Vancouver V5Z 4H4, BC, Canada | Department of Neurological Surgery, University of California, San Francisco, CA, USA | Department of Obstetrics and Gynecology, University of California, San Francisco, CA, USA
Note: [] MD, Clinical Professor and Head, British Columbia's Research Institute, Room 170, 950 West 28th Avenue, Vancouver V5Z 4H4, Canada. Tel.: +1 604 875 2345 (ext 6597); Fax: +1 604 875 3231; E-mail: [email protected]
Abstract: Glutathione peroxidase (GPx-1) is a selenoenzyme that metabolizes H_2O_2, a source of potentially toxic free radicals. Steroidogenesis is markedly inhibited by H_2O_2 in vitro. {\it Objective:} to study the effects of selenium deficiency on GPx activity and adrenal steroidogenesis in a novel adrenal cell line developed using targeted tumorigenesis. {\it Methods:} AN4Rppc7 cells were grown for 7 days in serum-free medium. 8-Br-cAMP-stimulated concentrations of steroid hormones were measured by RIA. StAR (Steroid Acute Reactive Protein) mRNA was measured by Northern blot. {\it Results:} selenium deficiency caused a 99% There was a 51%, progesterone, corticosterone and aldosterone production, respectivelyp<0.05 by ANOVA). StAR mRNA was not affected by selenium. {\it Conclusions:} selenium deficiency causes a marked decrease in GPx activity. Decreased steroid hormone production occurs for selenium concentrations equal or lower than 5 nM. The absence of changes in StAR mRNA content suggests that selenium deficiency does not affect cholesterol access to the mitochondria.
Keywords: glutathione peroxidase activity, selenium, adrenal cells, steroidogenesis, H[TeX:] _2O[TeX:] _2
Journal: BioFactors, vol. 14, no. 1-4, pp. 229-238, 2001
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