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

• Published in: Cell calcium (Edinburgh) Vol. 40; no. 4; pp. 347 - 357
• Main Authors: Koncz, Péter, Szanda, Gergo, Rajki, Anikó, Spät, András
• Format: Journal Article
• Language: English
• Published: Netherlands 01.10.2006
• Subjects: Angiotensin II - metabolism; Animals; Calcium Signaling - physiology; Cells, Cultured; Hydrogen Peroxide - pharmacology; Inositol 1,4,5-Trisphosphate - metabolism; Male; Membrane Potentials - radiation effects; Mitochondria - metabolism; NADP - metabolism; Oxidants - pharmacology; Potassium - metabolism; Pyridines - metabolism; Rats; Rats, Wistar; Reactive Oxygen Species - metabolism; Superoxides - metabolism; Ultraviolet Rays; Xanthine - metabolism; Xanthine Oxidase - metabolism; Zona Glomerulosa - cytology; Zona Glomerulosa - drug effects; Zona Glomerulosa - metabolism; Zona Glomerulosa - radiation effects
• ISSN: 0143-4160
• DOI: 10.1016/j.ceca.2006.04.003

The acute effects of ultraviolet light, the superoxide-generating xanthine-xanthine oxidase system and H(2)O(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(2)O(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.