Abstract

Publisher Summary Various studies have attempted to define the nature of the active oxygen intermediates involved in ultraviolet A (UVA) effects. From a series of experiments with different modifying agents, it was concluded that singlet oxygen was involved in the inactivation of cultured human skin fibroblasts that had been irradiated with near-monochromatic UV or near-visible radiation. Later it was shown that UVA activation of the heme oxygenase gene, that is the strongest UVA-activable response observed in eukaryotic cells, is also apparently mediated by singlet oxygen generated intracellularly by UVA radiation. Shortly afterward, the collagenase gene, known to be UVA inducible, could be activated by singlet oxygen liberated by thermal decomposition of a thermolabile endoperoxide. Since then it has been shown that singlet oxygen is probably involved in other examples of UVA-inducible gene expression. Not unexpectedly, singlet oxygen has now been implicated in UVA-mediated signal transduction pathways, including p38 and c-jun-N-terminal kinases but not extracellular regulated kinasesn; UVA also activates certain transcription factors. Singlet oxygen has been implicated in UVA induction of oxidative DNA damage. The approaches that implicate singlet oxygen in UVA-mediated events are necessarily indirect but generally include several lines of supporting evidence showing that singlet oxygen can be a mediator of the event concerned.

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