Role of mitochondria in ultraviolet-induced oxidative stress

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Abstract
The biological effects of ultraviolet radiation (UV), such as DNA damage, mutagenesis, cellular aging, and carcinogenesis, are in part mediated by reactive oxygen species (ROS). The major intracellular ROS intermediate is hydrogen peroxide, which is synthesized from superoxide anion (•O2−) and further metabolized into the highly reactive hydroxyl radical. In this study, we examined the involvement of mitochondria in the UV‐induced H2O2 accumulation in a keratinocyte cell line HaCaT. Respiratory chain blockers (cyanide‐p‐trifluoromethoxy‐phenylhydrazone and oligomycin) and the complex II inhibitor (theonyltrifluoroacetone) prevented H2O2 accumulation after UV. Antimycin A that inhibits electron flow from mitochondrial complex III to complex IV increased the UV‐induced H2O2 synthesis. The same effect was seen after incubation with rotenone, which blocks electron flow from NADH‐reductase (complex I) to ubiquinone. UV irradiation did not affect mitochondrial transmembrane potential (ΔΨm). These data indicate that UV‐induced ROS are produced at complex III via complex II (succinate‐Q‐reductase). J. Cell. Biochem. 80:216–222, 2000.