Abstract
Abstract Cigarette smoke, either directly or indirectly, causes alpha-1-proteinase inhibitor (a1PI) to lose elastase inhibitory capacity (EIC), leaving lung connective tissues susceptible to proteolytic degradation. This paper discusses possible mechanisms for inactivation by cigarette smoke (CS) and by a model system [NO, isoprene, and air] that duplicates much of CS free radical chemistry. Inactivation of a1PI by either CS or the model is biphasic; a fast inactivation is followed by a slower one. With pre-prepared extracts, only the slow inactivation is observed. Apparently short-lived species in the smoke itself and the model system cause the fast inactivation; they may be peroxynitrates, which form in smoke from nitrogen dioxide and peroxyl radicals. The slower inactivation appears to involve hydrogen peroxide and/or organic hydroperoxides or species produced by them. Incubation of a1PI with linoleic acid produces a slow loss of EIC, prevented by the presence of vitamin E, which supports the hypothesis of a route involving lipid hydroperoxides. Protection of a1PI by various types of compounds shows that unprotonated amines and amino acids protect, but the protonated or acylated compounds do not. Ascorbate and glutathione provide the strongest protection.
Published Version
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