Reactive oxygen species, Ca2+ signaling and mitochondrial NAD(P)H level in adrenal glomerulosa cells

The acute effects of ultraviolet light, the superoxide-generating xanthine–xanthine oxidase system and H2O2 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 H2O2, decreased the level of mitochondrial NAD(P)H. Free radical scavengers antagonized this effect of UV light. Extracellularly generated superoxide elicited Ca2+ transients and inhibited angiotensin II-induced cytoplasmic Ca2+ signaling. Low intensity UV light did not affect basal [Ca2+] and failed to influence Ca2+ signaling induced by depolarization or store depletion. UV light of the same low power reduced both cytoplasmic and mitochondrial Ca2+ signals induced by angiotensin II. The lack of UV effect on inositol phosphate formation indicates that the inhibition of cytoplasmic Ca2+ signaling is due to reduced Ca2+ release from InsP3-sensitive stores. Decreased mitochondrial Ca2+ uptake may be attributed to UV-induced perturbation of the perimitochondrial microdomain.