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Modeling oxidative stress in vitro with 5мМ H2O2 has demonstrated a protective role of nitric oxide on realization of constitutional blood neutrophil cell death. The NO-synthase inductor L-arginine and the inhibitor of nitric oxide synthesis, L-NAME, influenced on the amount of annexin-positive cells, the content of Bax protein, reactive oxygen species, cyclic nucleotides, and calcium homeostasis in neutrophils under conditions realizing programmed death during oxidative stress in vitro and under acute inflammation. During oxidative stress L-arginine normalized the increased intracellular Ca2+ level and the cАМP/cGМP ratio due to increase of cGМP level, stabilized metabolism and prolonged neutrophil life. During acute inflammation NO induction was insufficient for limitation of Ca2+ release into cytosol and for onset of the apoptotic effect; blockade of NO synthesis deteriorated this situation by activating neutrophil apoptosis due to the sharp increase in Ca2+ content and reduction of cyclic nucleotides in cytosol. The protective effect of NO on neutrophil cell death during oxidative dysbalance is not associated with regulation of apoptotic protein Bax.

The role of nitric oxide synthesis induction and inhibition in regulation of blood neutrophil cell death during oxidative disbalance