Mitochondrial electron transport chain activity is not involved in ultraviolet A (UVA)-induced cell death |
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| Authors: | Schauen Matthias Hornig-Do Hue-Tran Schomberg Sarah Herrmann Gernot Wiesner Rudolf J |
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| Institution: | 1. Institute of Vegetative Physiology, University of Köln, Robert-Koch-Strasse 39, 50924 Köln, Germany;2. Department of Dermatology, University of Köln, Köln, Germany;3. Center for Molecular Medicine Cologne (CMMC), University of Köln, Köln, Germany;1. Seoul Regional Food & Drug Administration, Ministry of Food and Drug Safety, 212, Mokdongjungang-ro, Yangcheon-gu, Seoul, Republic of Korea;2. Graduate School of Pharmaceutical Sciences, Ewha Womans University, 52 Ewhayeodae-gil, Seodaemun-gu, Seoul, Republic of Korea;3. Pharmaceutical and Medical Devices Research Department, Ministry of Food and Drug Safety, Osong Health Technology Administration Complex, 643 Yeonje-ri, Gangoe-myeon, Cheongwon-gun, Chungcheongbuk-do, Republic of Korea;1. Department of Chemistry and Biochemistry, ISES Labs, Russell Sage College, Troy, NY 12180, USA;2. Department of Chemistry and Chemical Biology, Rensselaer Polytechnic Institute, Troy, NY 12180, USA;1. Breast Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, 300 E. 66th St., New York, NY, 10065, USA;2. Department of Pathology, A.C. Camargo Cancer Center, Sao Paulo, Brazil;3. Department of Epidemiology and Biostatistics, Memorial Sloan Kettering Cancer Center, New York, NY, 10065, USA;4. Sloan-Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, NY, 10065, USA;5. Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, NY, 10065, USA;6. Genomics Core, Memorial Sloan Kettering Cancer Center, New York, NY, 10065, USA |
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| Abstract: | 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. |
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