It was previously observed that lipid membranes accelerate .NO disappearance (Liu et al. (1998) Proc. Natl. Acad. Sci. U.S.A. 95, 2175), and here, we demonstrate that this translates into increased rates of .NO2 production and nitrosative chemistry. Not only the phospholipid membranes but also the atherosclerosis-related low-density lipoprotein (LDL) were able to accelerate the formation of .NO 2, studied by stopped-flow spectrophotometry using ABTS as a probe. In addition, membranes, LDL, and Triton X-100 micelles significantly accelerated S-nitrosation of glutathione and captopril. It is shown here that autoxidation of .NO occurs 30 times more rapidly within the hydrophobic interior of these particles than in an equal volume of water, approximately 1 order of magnitude less than previous reports. This acceleration can be explained by the ∼3 times higher solubility of .NO and O2 into these hydrophobic phases relative to water, which results in a higher local concentration of reactants ("lens effect") and, therefore, a higher rate of reaction. It is predicted that 50% of the oxidizing and nitrosating species derived from .NO autoxidation in cells will be formed in the small volume comprising cellular membranes (3% of the total); thus, biomolecules near the membranes will be exposed to fluxes of reactive nitrogen species 30-fold higher than their cytosolic counterparts. © 2007 American Chemical Society.
