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谷胱甘肽耗竭对无毛小鼠晒伤细胞形成的影响。

Effect of glutathione depletion on sunburn cell formation in the hairless mouse.

作者信息

Hanada K, Gange R W, Connor M J

机构信息

Wellman Laboratories, Department of Dermatology, Harvard Medical School, Boston, MA 02114.

出版信息

J Invest Dermatol. 1991 Jun;96(6):838-40. doi: 10.1111/1523-1747.ep12474538.

Abstract

Cutaneous protection against ultraviolet B (UVB) radiation damage by endogenous glutathione (GSH) was evaluated in the epidermis of the hairless mouse by measuring the influence of GSH depletion on sunburn cell (SBC) formation. Cellular GSH exerts antioxidant effects and recent studies have suggested a role for oxygen radicals in the production of SBC. Hairless mice (Skh/h 1) received oral treatment with buthionine S,R-sulfoximine (BSO), an irreversible inhibitor of gamma-glutamylcysteine synthetase, to deplete cutaneous GSH; 4 d later their ears were exposed to UVB radiation. BSO treatment significantly reduced GSH levels in the epidermis to 10-15% of control levels. Twenty-four hours after UVB exposure, SBC counts in the ears of animals with and without BSO treatment were measured, and those exposed to UVB were found to have increased. Greater numbers of SBC were found in the ears of BSO-treated mice exposed to 15 or 20 mJ/cm2 UVB, than in non-BSO-treated mice exposed to the same UVB doses. At higher UVB doses, there were no statistically significant differences between the groups. The results show that endogenous GSH provides the epidermis with measurable protection against injury by low or moderate UVB doses.

摘要

通过测量谷胱甘肽(GSH)耗竭对晒伤细胞(SBC)形成的影响,在无毛小鼠的表皮中评估内源性GSH对紫外线B(UVB)辐射损伤的皮肤保护作用。细胞内的GSH具有抗氧化作用,最近的研究表明氧自由基在SBC的产生中起作用。无毛小鼠(Skh/h 1)口服丁硫氨酸S,R-亚砜亚胺(BSO),一种γ-谷氨酰半胱氨酸合成酶的不可逆抑制剂,以耗尽皮肤中的GSH;4天后,它们的耳朵暴露于UVB辐射下。BSO处理显著降低了表皮中的GSH水平,使其降至对照水平的10%-15%。UVB照射24小时后,测量了经BSO处理和未经BSO处理的动物耳朵中的SBC计数,发现暴露于UVB的动物的SBC计数增加。在暴露于15或20 mJ/cm2 UVB的BSO处理小鼠的耳朵中,发现的SBC数量比暴露于相同UVB剂量的非BSO处理小鼠的耳朵中更多。在较高的UVB剂量下,两组之间没有统计学上的显著差异。结果表明,内源性GSH为表皮提供了可测量的保护,使其免受低或中等剂量UVB的损伤。

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