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, O2 {dot minus} 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 O2 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 O2 {dot minus} 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) O2 {dot minus} is probably generated in the upper and lower respiratory tract lining fluid when they come in contact with CS; (ii) such generated O2 {dot minus} 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.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 30-37 |
| Number of pages | 8 |
| Journal | Archives of Biochemistry and Biophysics |
| Volume | 299 |
| Issue number | 1 |
| DOIs | |
| State | Published - Nov 15 1992 |
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ASJC Scopus subject areas
- Biochemistry
- Biophysics
- Molecular Biology
Cite this
Superoxide formed from cigarette smoke impairs polymorphonuclear leukocyte active oxygen generation activity. / Tsuchiya, Masahiko; Thompson, David F T; Suzuki, Yuichiro J.; Cross, Carroll E; Packer, Lester.
In: Archives of Biochemistry and Biophysics, Vol. 299, No. 1, 15.11.1992, p. 30-37.Research output: Contribution to journal › Article
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TY - JOUR
T1 - Superoxide formed from cigarette smoke impairs polymorphonuclear leukocyte active oxygen generation activity
AU - Tsuchiya, Masahiko
AU - Thompson, David F T
AU - Suzuki, Yuichiro J.
AU - Cross, Carroll E
AU - Packer, Lester
PY - 1992/11/15
Y1 - 1992/11/15
N2 - 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, O2 {dot minus} 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 O2 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 O2 {dot minus} 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) O2 {dot minus} is probably generated in the upper and lower respiratory tract lining fluid when they come in contact with CS; (ii) such generated O2 {dot minus} 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.
AB - 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, O2 {dot minus} 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 O2 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 O2 {dot minus} 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) O2 {dot minus} is probably generated in the upper and lower respiratory tract lining fluid when they come in contact with CS; (ii) such generated O2 {dot minus} 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.
UR - http://www.scopus.com/inward/record.url?scp=0026437385&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0026437385&partnerID=8YFLogxK
U2 - 10.1016/0003-9861(92)90240-W
DO - 10.1016/0003-9861(92)90240-W
M3 - Article
C2 - 1332616
AN - SCOPUS:0026437385
VL - 299
SP - 30
EP - 37
JO - Archives of Biochemistry and Biophysics
JF - Archives of Biochemistry and Biophysics
SN - 0003-9861
IS - 1
ER -