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Superoxide formed from cigarette smoke impairs polymorphonuclear leukocyte active oxygen generation activity
M Tsuchiya1, D F Thompson, Y J Suzuki
1Department of Molecular and Cell Biology, University of California, Berkeley 94720.
Archives of Biochemistry and Biophysics
|November 15, 1992
Summary
Cigarette smoke impairs immune cells like polymorphonuclear leukocytes (PMNs) by generating superoxide radicals. Antioxidants may protect against these harmful effects in lung diseases.
Area of Science:
- Pulmonary Medicine
- Immunology
- Toxicology
Background:
- Cigarette smoke (CS) contains reactive free radicals implicated in lung disease pathogenesis.
- Impaired phagocytic antimicrobial activities, particularly of polymorphonuclear leukocytes (PMNs), contribute to CS-related pulmonary disorders.
Purpose of the Study:
- To investigate the impact of CS-generated reactive oxygen species on PMN function.
- To identify the specific reactive oxygen species involved and explore potential protective strategies.
Main Methods:
- CS-exposed buffer solutions were analyzed for reactive oxygen species using lucigenin-amplified chemiluminescence and ESR spin-trapping.
- PMNs were incubated in CS-exposed buffer and their stimulated active oxygen production and O2 consumption were measured.
- The protective effects of superoxide dismutase (SOD), an iron chelator (DETAPAC), and antioxidants (alpha-tocopherol, DHLA) were assessed.
Main Results:
- Superoxide anion (O2-.) was the predominant reactive oxygen species generated in CS-exposed solutions.
- PMN function, including active oxygen production, was significantly impaired by CS exposure, with 75% inhibition after 1-min exposure.
- SOD and DETAPAC provided complete protection, while alpha-tocopherol and dihydrolipoic acid (DHLA) offered partial protection to PMNs.
Conclusions:
- CS exposure likely generates O2-. in respiratory tract lining fluid, impairing PMN antimicrobial capabilities.
- O2-. appears to be an initiating factor, with hydroxyl radical (OH.) generation as a subsequent injurious factor.
- Antioxidant supplementation with alpha-tocopherol or DHLA may prevent CS-induced PMN dysfunction and contribute to preventing CS-related lung diseases.