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紫外线B对渔游蛇(Elaphe taeniura)表皮形态、蜕皮、脂质过氧化物和抗氧化酶的影响。

Effects of ultraviolet B on epidermal morphology, shedding, lipid peroxide, and antioxidant enzymes in Cope's rat snake (Elaphe taeniura).

作者信息

Chang Cheng, Zheng Rongliang

机构信息

School of Life Sciences, Lanzhou University, Lanzhou 730000, China.

出版信息

J Photochem Photobiol B. 2003 Dec 5;72(1-3):79-85. doi: 10.1016/j.jphotobiol.2003.06.001.

DOI:10.1016/j.jphotobiol.2003.06.001
PMID:14644569
Abstract

Cope's rat snakes (Elaphe taeniura) favor to expose under sunlight in order to increase their body temperature simultaneously increasing the risk of skin damage by ultraviolet B (UVB) irradiation. We have investigated the effects of UVB irradiation on their skin. Results show that the UVB transmission of the keratinous layer was only 5.1+/-0.36%. The peak of epidermal damage and malondialdehyde (MDA) content, a product of lipid peroxidation, simultaneously occurred 72-96, 48 or 24 h after exposure to 300, 500 and 800 mJ/cm2 of UVB radiation, respectively. Superoxide dismutase (SOD) activity was inhibited by UVB and the lowest activity occurred 24, 48, 12 and 12 h after exposure to 110, 300, 500 and 800 mJ/cm2 of UVB, respectively. SOD activity recovered later to some extent but mostly remained below control level. After exposure to different doses of UVB radiation, catalase (CAT) activity was inhibited immediately, and then gradually recovered and even increased to peak levels above control level. The highest CAT levels accompanied the most serious damage of skin morphology. Later on, CAT activity decreased and recovered again close to or below control level, which was accompanied by shedding off the damaged epidermal complex. This indicated that the epidermal damage induced by UVB is closely related to lipid peroxidation, where CAT acts as a primary antioxidant enzyme. Moreover, the keratinous layer protects the viable cell layer against UVB damage as well.

摘要

柯氏滑鼠蛇(锦蛇属)喜欢在阳光下晒太阳以提高体温,同时这也增加了被紫外线B(UVB)辐射损伤皮肤的风险。我们研究了UVB辐射对其皮肤的影响。结果表明,角质层的UVB透过率仅为5.1±0.36%。表皮损伤峰值和脂质过氧化产物丙二醛(MDA)含量分别在暴露于300、500和800 mJ/cm² 的UVB辐射后72 - 96小时、48小时或24小时同时出现。超氧化物歧化酶(SOD)活性受到UVB抑制,分别在暴露于110、300、500和800 mJ/cm² 的UVB后24小时、48小时、12小时和12小时出现最低活性。SOD活性随后在一定程度上恢复,但大多仍低于对照水平。暴露于不同剂量的UVB辐射后,过氧化氢酶(CAT)活性立即受到抑制,然后逐渐恢复,甚至升高至高于对照水平的峰值。最高的CAT水平伴随着最严重的皮肤形态损伤。随后,CAT活性下降并再次恢复至接近或低于对照水平,同时受损的表皮复合物脱落。这表明UVB诱导的表皮损伤与脂质过氧化密切相关,其中CAT作为主要的抗氧化酶。此外,角质层也保护活细胞层免受UVB损伤。

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