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Abstract Number: 5668
Effects of dietary selenium compounds and glutathione modifiers on epidermal reduced glutathione in the ultraviolet light-exposed Skh:HR-1 mouse model
Chwan-Li Shen, Woosun Song, Barbara C. Pence, Texas Tech University Health Sciences Center, Lubbock, TX.
We have previously reported that the in vitro pro-apoptotic effects of selenite (SeL) are dependent on the concentration of intracellular reduced glutathione (GSH). The present study was designed to investigate the GSH-dependent effects of Se compounds in the skin of hairless mice.
A total of 80 female 5 to 7 week old Skh:HR-1 hairless mice were randomly divided into four dietary groups and were fed one of four test diets containing either no selenium (Se), 0.5 ppm Se as SeL, 0.5 ppm Se as selenomethionine (SeM), or 0.5 ppm Se as Se-methylselenocysteine (SeMC) for 4 weeks.
To alter the concentration of intracellular GSH, mice were given either GSH monoester (25 mg/mouse) by gavage 4 hr prior to ultraviolet light (UVB) exposure or buthionine sulfoximine (BSO, 2 mg/ml) in the drinking water for four days prior to and one day after exposure to UVB at 90 mJ/cm2.
Ten mice from each diet were sacrificed with either no UVB exposure or 24 h after a single UVB exposure. Strips of dorsal skin were collected from mice and epidermal cells scraped from the skin for the measurement of GSH.
Supplemental GSH prior to exposure to UVB decreased epidermal GSH in all groups, and dietary groups maintained their GSH status after UVB in the following order: SeL>no Se>SeMC>SeM. Following BSO treatment and UVB exposure, those with no UVB exposure maintained GSH status better than the UVB exposed groups. Test diets maintained GSH in the order: no Se>SeM>SeL>SeMC.
These data demonstrated that GSH status is important in the response to UVB damage, and that the enhanced GSH synthesis usually seen with SeMC is suppressed by either supplemental GSH or by inhibition of GSH synthesis. The relationship of GSH to Se may be critical to chemoprevention strategies.
Supported by NIH, CA 76675.
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