The autoxidation of NO leads to the formation of NO₂ and N₂O₃, strong oxidative and nitrosative species. This reaction was considered to be too slow to be relevant in biological media until Liu et al. reported that hydrophobic compartments can accelerate the reaction of nitric oxide (NO) with O2 (autoxidation) approximately 300 times within the hydrophobic compartment (Liu PNAS 95, 2175) and now it is often regarded as an important source of nitrosative chemistry. We were particularly interested in assessing the capacity of a relevant biomedical lipid particle such as low density lipoprotein (LDL) in accelerating this reaction. LDL is involved in cholesterol transport and a great amount of evidence indicates that its oxidation is one of the initial events in the development of arteriosclerosis. Other hydrophobic particles, such as lecithin liposomes and Triton X-100 micelles were assayed for comparison. The NO autoxidation was followed electrochemically with an NO-selective electrode and it was found that this reaction was accelerated about 30 times within these hydrophobic particles (one order of magnitude lower than reported by Liu). To confirm our observations, the formation of the immediate product of NO autoxidation NO₂ was studied by ABTS oxidation and stopped-flow spectrophotometry, supporting a ~30 times faster NO autoxidation. We recently determined the partition coefficients for NO and O₂ within these hydrophobic particles (Kp ~ 3, Moller JBC 280, 8850) and theoretical models indicate that the acceleration is mainly due to the higher NO and O₂ solubility within hydrophobic media rather than changes in the intrinsic rate constant. Since NO autoxidation leads to oxidative species formation, the effects of NO autoxidation on LDL were studied and found a mild lipid oxidation while the main modification was thiol nitrosation, pointing to the LDL thiols as important kinetic targets of reactive nitrogen species.