Ambient particulate air pollution from vehicles promotes lipid peroxidation and inflammatory responses in rat lung
Oxidative stress plays a major role in the pathogenesis of particle-dependent lung injury. Ambient particle levels from vehicles have not been previously shown to cause oxidative stress to the lungs. The present study was conducted to a) determine whether short-term exposure to ambient levels of par...
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Associação Brasileira de Divulgação Científica
2007-10-01
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Online Access: | http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2007001000008 |
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doaj-7b9bc64e32a44d61b72e046cda0aa9152020-11-24T23:16:53ZengAssociação Brasileira de Divulgação CientíficaBrazilian Journal of Medical and Biological Research0100-879X1414-431X2007-10-01401013531359Ambient particulate air pollution from vehicles promotes lipid peroxidation and inflammatory responses in rat lungC.E.L. PereiraT.G. HeckP.H.N. SaldivaC.R. RhodenOxidative stress plays a major role in the pathogenesis of particle-dependent lung injury. Ambient particle levels from vehicles have not been previously shown to cause oxidative stress to the lungs. The present study was conducted to a) determine whether short-term exposure to ambient levels of particulate air pollution from vehicles elicits inflammatory responses and lipid peroxidation in rat lungs, and b) determine if intermittent short-term exposures (every 4 days) induce some degree of tolerance. Three-month-old male Wistar rats were exposed to ambient particulate matter (PM) from vehicles (N = 30) for 6 or 20 continuous hours, or for intermittent (5 h) periods during 20 h for 4 consecutive days or to filtered air (PM <10 µm; N = 30). Rats continuously breathing polluted air for 20 h (P-20) showed a significant increase in the total number of leukocytes in bronchoalveolar lavage compared to control (C-20: 2.61 x 105 ± 0.51;P-20: 5.01 x 105 ± 0.81; P < 0.05) and in lipid peroxidation ([MDA] nmol/mg protein: C-20: 0.148 ± 0.01; P-20: 0.226 ± 0.02; P < 0.05). Shorter exposure (6 h) and intermittent 5-h exposures over a period of 4 days did not cause significant changes in leukocytes. Lipid damage resulting from 20-h exposure to particulate air pollution did not cause a significant increase in lung water content. These data suggest oxidative stress as one of the mechanisms responsible for the acute adverse respiratory effects of particles, and suggest that short-term inhalation of ambient particulate air pollution from street with high automobile traffic represents a biological hazard.http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2007001000008Oxidative stressReactive oxygen speciesLipid peroxidationParticulate air pollutionLung inflammationAcute effects |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
C.E.L. Pereira T.G. Heck P.H.N. Saldiva C.R. Rhoden |
spellingShingle |
C.E.L. Pereira T.G. Heck P.H.N. Saldiva C.R. Rhoden Ambient particulate air pollution from vehicles promotes lipid peroxidation and inflammatory responses in rat lung Brazilian Journal of Medical and Biological Research Oxidative stress Reactive oxygen species Lipid peroxidation Particulate air pollution Lung inflammation Acute effects |
author_facet |
C.E.L. Pereira T.G. Heck P.H.N. Saldiva C.R. Rhoden |
author_sort |
C.E.L. Pereira |
title |
Ambient particulate air pollution from vehicles promotes lipid peroxidation and inflammatory responses in rat lung |
title_short |
Ambient particulate air pollution from vehicles promotes lipid peroxidation and inflammatory responses in rat lung |
title_full |
Ambient particulate air pollution from vehicles promotes lipid peroxidation and inflammatory responses in rat lung |
title_fullStr |
Ambient particulate air pollution from vehicles promotes lipid peroxidation and inflammatory responses in rat lung |
title_full_unstemmed |
Ambient particulate air pollution from vehicles promotes lipid peroxidation and inflammatory responses in rat lung |
title_sort |
ambient particulate air pollution from vehicles promotes lipid peroxidation and inflammatory responses in rat lung |
publisher |
Associação Brasileira de Divulgação Científica |
series |
Brazilian Journal of Medical and Biological Research |
issn |
0100-879X 1414-431X |
publishDate |
2007-10-01 |
description |
Oxidative stress plays a major role in the pathogenesis of particle-dependent lung injury. Ambient particle levels from vehicles have not been previously shown to cause oxidative stress to the lungs. The present study was conducted to a) determine whether short-term exposure to ambient levels of particulate air pollution from vehicles elicits inflammatory responses and lipid peroxidation in rat lungs, and b) determine if intermittent short-term exposures (every 4 days) induce some degree of tolerance. Three-month-old male Wistar rats were exposed to ambient particulate matter (PM) from vehicles (N = 30) for 6 or 20 continuous hours, or for intermittent (5 h) periods during 20 h for 4 consecutive days or to filtered air (PM <10 µm; N = 30). Rats continuously breathing polluted air for 20 h (P-20) showed a significant increase in the total number of leukocytes in bronchoalveolar lavage compared to control (C-20: 2.61 x 105 ± 0.51;P-20: 5.01 x 105 ± 0.81; P < 0.05) and in lipid peroxidation ([MDA] nmol/mg protein: C-20: 0.148 ± 0.01; P-20: 0.226 ± 0.02; P < 0.05). Shorter exposure (6 h) and intermittent 5-h exposures over a period of 4 days did not cause significant changes in leukocytes. Lipid damage resulting from 20-h exposure to particulate air pollution did not cause a significant increase in lung water content. These data suggest oxidative stress as one of the mechanisms responsible for the acute adverse respiratory effects of particles, and suggest that short-term inhalation of ambient particulate air pollution from street with high automobile traffic represents a biological hazard. |
topic |
Oxidative stress Reactive oxygen species Lipid peroxidation Particulate air pollution Lung inflammation Acute effects |
url |
http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2007001000008 |
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