Decrease of antioxidants and the formation of oxidized diacylglycerol in mouse skin caused by UV irradiation

Yutaka Tanino , Arief Budiyanto , Masato Ueda , Akihiro Nakada , Wei Tak Nyou , Makoto Yanagisawa , Masamitsu Ichihashi , Yorihiro Yamamoto
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引用次数: 8

Abstract

UV irradiation induces inflammation and immunosuppression, and may cause skin cancer. To elucidate the molecular mechanism of these pathological events we exposed hairless mice to UVA at a dose of 5 J/cm2. It resulted in the decay of ascorbate, urate, and reduced form of coenzyme Q, and the formation of oxidized diacylglycerols which can activate protein kinase C and human neutrophils. UVB irradiation also caused the decay of ascorbate and urate, and the formation of oxidized diacylglycerols. These results show that the irradiation of both UVA and UVB induces free radical oxidation of antioxidants and lipids, and indicate that oxidized diacylglycerols may play a role as an endogenous tumor promoter in UV-induced skin carcinogenesis.

紫外线照射引起小鼠皮肤抗氧化剂的减少和氧化二酰基甘油的形成
紫外线照射会引起炎症和免疫抑制,并可能导致皮肤癌。为了阐明这些病理事件的分子机制,我们将无毛小鼠暴露在5j /cm2剂量的UVA下。它导致抗坏血酸盐、尿酸盐的衰变和辅酶Q的还原形式,并形成氧化的二酰基甘油,可以激活蛋白激酶C和人类中性粒细胞。UVB辐照还引起抗坏血酸盐和尿酸盐的衰变,并形成氧化的二酰基甘油。上述结果表明,UVA和UVB照射均可诱导自由基氧化抗氧化剂和脂质,氧化二酰基甘油可能在紫外线诱导的皮肤癌变中发挥内源性肿瘤促进剂的作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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