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超氧阴离子可能介导紫外线辐射对黑素生成的短期而非长期影响。

The superoxide anion may mediate short- but not long-term effects of ultraviolet radiation on melanogenesis.

作者信息

Tobin D, Thody A J

机构信息

Department of Dermatology, University of Newcastle upon Tyne, Royal Victoria Infirmary, UK.

出版信息

Exp Dermatol. 1994 Jun;3(3):99-105. doi: 10.1111/j.1600-0625.1994.tb00266.x.

DOI:10.1111/j.1600-0625.1994.tb00266.x
PMID:7952923
Abstract

The present study was carried out to examine the role of reactive oxygen species in mediating the melanogenic effects of UVR. B16 mouse melanoma cells responded to a single dose of UVR by showing increases in their melanin content. Although there was a small increase in melanin at 48-72 hours, which was associated with a rise in tyrosinase activity at 48 h, the greatest change occurred at 3 h and this was not associated with an increase in tyrosinase activity. This short-term response, unlike the more delayed melanogenic response, was reduced by superoxide dismutase (SOD). Xanthine oxidase (XO), which generates the superoxide anion (O2-), also increased the melanin content of B16 melanoma cells with effects at 3 h and 48 h. As with UVR, the delayed response was accompanied by an increase in tyrosinase activity but no such association was evident at 3 h. In addition, the short-term effect, like that seen with UVR, was reduced with SOD and to a lesser extent with catalase. In contrast to the effects found with XO, glucose oxidase, which generates hydrogen peroxide, had no effect on the melanin content or tyrosinase activity of the B16 cells. These results confirm previous observations that UVR is able to act directly on cells to bring about delayed increases in melanogenesis. They further demonstrate that UVR also stimulates melanogenesis through a more rapid action that is not associated with an activation of tyrosinase. This effect could be mediated by the O2- which, rather than activating tyrosinase, could act by serving as a substrate for the enzyme.

摘要

本研究旨在探讨活性氧在介导紫外线辐射(UVR)致黑素生成效应中的作用。B16小鼠黑色素瘤细胞对单次UVR照射有反应,其黑色素含量增加。虽然在48 - 72小时黑色素有小幅增加,且与48小时酪氨酸酶活性升高有关,但最大变化发生在3小时,且这与酪氨酸酶活性增加无关。与更延迟的黑素生成反应不同,这种短期反应可被超氧化物歧化酶(SOD)减弱。产生超氧阴离子(O2-)的黄嘌呤氧化酶(XO)也增加了B16黑色素瘤细胞的黑色素含量,在3小时和48小时均有作用。与UVR一样,延迟反应伴随着酪氨酸酶活性增加,但在3小时时无明显关联。此外,短期效应与UVR作用相似,可被SOD减弱,而过氧化氢酶的减弱作用较小。与XO的作用相反,产生过氧化氢的葡萄糖氧化酶对B16细胞的黑色素含量或酪氨酸酶活性无影响。这些结果证实了先前的观察结果,即UVR能够直接作用于细胞,导致黑素生成延迟增加。它们进一步证明,UVR还通过一种与酪氨酸酶激活无关的更快作用来刺激黑素生成。这种效应可能由O2-介导,O2-不是激活酪氨酸酶,而是作为该酶的底物起作用。

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