Abstract

Reactive free radicals contained in cigarette smoke (CS) and compromised phagocytic antimicrobial activities including those of polymorphonuclear leukocytes (PMNs) have been implicated in the pathogenesis of severe CS-related pulmonary disorders. In CS-exposed buffer solutions, O 2 ∸ was the predominant generated reactive oxygen species, as demonstrated by lucigenin-amplified chemiluminescence and electron spin resonance (ESR) spin-trapping with 5,5-dimethyl-1-pyrroline N-oxide (DMPO). When PMNs were incubated in this buffer, phorbol 12-myristate 13-acetate (PMA)-stimulated active oxygen production and coupled O 2 consumption were strongly impaired without appreciably affecting PMN viability (1-min exposure inhibited active oxygen production by 75%). Superoxide dismutase (SOD) totally protected and an iron chelator, diethylenetriaminepentaacetic acid (DETAPAC), also protected the CS-exposed PMNs, suggesting that generated O 2 ∸ was an initiating factor in the impairment and OH · generation was a subsequent injurious factor. Pretreatment of PMNs with antioxidants such as α-tocopherol and dihydrolipoic acid (DHLA) was partially protective. The results suggest that (i) O 2 ∸ is probably generated in the upper and lower respiratory tract lining fluid when they come in contact with CS; (ii) such generated O 2 ∸ can primarily impair PMN capabilities to generate reactive oxygen species; and (iii) since these effects may contribute to the pathogenesis of CS-related lung diseases, prior supplementation with antioxidants such as α-tocopherol or DHLA might be successful in preventing these deleterious effects.

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