The cytosolic calcium concentration is affected by S ‐nitrosocysteine in human lymphomonocytes

The homeostasis of cytosolic calcium [Ca 2+ ] c in mammalian cells is a complex phenomenon, requiring the contribution of many cellular and extracellular systems. Nitric oxide (NO) acts on [Ca 2+ ] c , although the mechanism of this action is unknown. We study the release and the uptake of Ca 2+ in the endoplasmic reticulum and its capacitative entry in human lymphomonocytes in the presence of the NO donor S ‐nitrosocysteine (CysNO) at low (16 μM) and at high (160 μM) concentrations by measuring the [Ca 2+ ] c by the Fura 2‐AM method. Thapsigargin (TG), which inhibits sarco‐endoplasmic reticulum Ca 2+ ‐ATPase (SERCA), and nifedipine (NIF), which blocks the Ca 2+ release from intracellular stores, are used to clarify the effects of NO on calcium movements. In the absence of extracellular Ca 2+ , CysNO decreases basal [Ca 2+ ] c , whereas TG increases it as the result of SERCA inhibition. This effect of TG diminishes in the presence of the NO donor. In the presence of extracellular Ca 2+ (capacitative entry conditions), CysNO does not influence Ca 2+ entry but reduces the toxic effects of TG connected to the increase of [Ca 2+ ] c in these conditions. The effect of NIF is, up to a certain extent, similar to that of CysNO, although the mechanisms of action of the two agents do not seem related. We conclude that CysNO participates in [Ca 2+ ] c homeostasis by stimulating the movement of the ion from the cytosol to other compartments. © 2008 Wiley Periodicals, Inc. J Biochem Mol Toxicol 22:35–40, 2008; Published online in Wiley InterScience ( www.interscience.wiley.com ). DOI 10.1002/jbt.20211