Mitochondrial electron transport chain activity is not involved in ultraviolet A (UVA)-induced cell death.
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.
Schauen
Matthias
M
Institute of Vegetative Physiology, University of Köln, Robert-Koch-Strasse 39, 50924 Köln, Germany. m.schauen@uni-koeln.de
Hornig-Do
Hue-Tran
HT
Schomberg
Sarah
S
Herrmann
Gernot
G
Wiesner
Rudolf J
RJ
D016923:Cell Death / Q000528:radiation effects*; D004579:Electron Transport; D005434:Flow Cytometry; D006367:HeLa Cells; D006801:Humans; D008928:Mitochondria / Q000378:metabolism / Q000528:radiation effects*; D010101:Oxygen Consumption; D017382:Reactive Oxygen Species; D014466:Ultraviolet Rays
D017382:Reactive Oxygen Species