Mitochondrial electron transport chain activity is not involved in ultraviolet A (UVA)-induced cell death

被引:39
|
作者
Schauen, Matthias
Hornig-Do, Hue-Tran
Schomberg, Sarah
Herrmann, Gernot
Wiesner, Rudolf J.
机构
[1] Univ Cologne, Inst Vegetat Physiol, D-50924 Cologne, Germany
[2] Univ Cologne, Dept Dermatol, D-50924 Cologne, Germany
[3] Univ Cologne, CMMC, D-50924 Cologne, Germany
关键词
UVA radiation; mitochondria; electron transport chain; respiration; mitochondrial DNA; ROS; fibroblasts; keratinocytes; diphenyleneiodonium; resiniferatoxin; plasma membrane oxidases;
D O I
10.1016/j.freeradbiomed.2006.11.016
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Ultraviolet A (UVA), the long wavelength part of the sun's ultraviolet radiation, elicits its harmful effects through production of reactive oxygen species. In this study, we have tested the hypothesis that the mitochondrial electron transport chain, the main source of reactive oxygen species in cells, importantly contributes to UVA-induced cell damage. Model cell lines completely lacking a mitochondrial electron transport chain (rho(0)-cells) were not protected against UVA-induced cell death. Also, primary human fibroblasts and keratinocytes with induced depletion of electron transport chain activity were not better protected against UVA-induced cell death. On the other hand, diphenyleneiodonium and resiniferatoxin, inhibitors of plasma membrane oxidases, protected primary human fibroblasts against UVA, as potently as the lipid peroxidation chain breaker Trolox. These data indicate that plasma membrane electron transport systems, but not the mitochondrial electron transport chain, play a major role in UVA-induced cell death. (c) 2006 Elsevier Inc. All rights reserved.
引用
收藏
页码:499 / 509
页数:11
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