Abstract
The acute effects of ultraviolet light, the superoxide-generating xanthine–xanthine oxidase system and H 2O 2 to on calcium signaling and mitochondrial pyridine nucleotide metabolism were investigated in rat glomerulosa cells. UV light induced the formation of superoxide, that, similar to exogenously applied superoxide and H 2O 2, decreased the level of mitochondrial NAD(P)H. Free radical scavengers antagonized this effect of UV light. Extracellularly generated superoxide elicited Ca 2+ transients and inhibited angiotensin II-induced cytoplasmic Ca 2+ signaling. Low intensity UV light did not affect basal [Ca 2+] and failed to influence Ca 2+ signaling induced by depolarization or store depletion. UV light of the same low power reduced both cytoplasmic and mitochondrial Ca 2+ signals induced by angiotensin II. The lack of UV effect on inositol phosphate formation indicates that the inhibition of cytoplasmic Ca 2+ signaling is due to reduced Ca 2+ release from InsP 3-sensitive stores. Decreased mitochondrial Ca 2+ uptake may be attributed to UV-induced perturbation of the perimitochondrial microdomain.
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