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In order for nitric oxide (NO) to function as a biological messenger it has to be inactivated, but little is known of how this is achieved. In cells from the brain, we have recently shown the existence of a powerful NO sink that 'shapes' NO signals for targeting its receptor, soluble guanylate cyclase, whilst simultaneously preventing NO rising to toxic concentrations [Griffiths and Garthwaite (2001) J. Physiol. (Cambridge, U.K.) 536, 855-862]. In the present study, the properties of this sink were investigated further. Inactivation of NO was preserved in rat brain homogenates. In both cerebellar cell suspensions and brain homogenates, NO inactivation required O(2) and, from measurements in homogenates, the principal end-product was NO(-)(3), which is also the main product of endogenously formed NO in vivo. Direct chemical reaction with O(2), superoxide anions or haemoglobin was not responsible. Consumption of NO was, however, inhibited by heat or protease treatment. Pharmacological tests were negative for several candidate enzymes, namely cytochrome c oxidase, H(2)O(2)-dependent haem peroxidases, prostaglandin H synthase, 12/15-lipoxygenase and a flavohaemoglobin-like NO dioxygenase. The capacity of the NO sink in cells was limited because regeneration of the activity was slow (2 h). It is concluded that NO is consumed in the brain through a novel protein, ultimately forming NO(-)(3), and that the slow regeneration of the activity provides a scenario for NO to become toxic.

Nitric oxide inactivation in brain by a novel O2-dependent mechanism resulting in the formation of nitrate ions