IBIMOL   23987
INSTITUTO DE BIOQUIMICA Y MEDICINA MOLECULAR PROFESOR ALBERTO BOVERIS
Unidad Ejecutora - UE
artículos
Título:
Low Doses of Urban Air Particles from Buenos Aires Promote Oxidative Stress and Apoptosis in Mice Lungs
Autor/es:
MARTIN, SUSANA; FERNANDEZ ALANIS, EUGENIO; DELFOSSE, VERONICA; EVELSON, PABLO; YAKISICH, SEBASTIAN; SALDIVA, PAULO; TASAT, DEBORAH
Revista:
INHALATION TOXICOLOGY
Editorial:
TAYLOR & FRANCIS INC
Referencias:
Año: 2011 p. 1064 - 1071
ISSN:
0895-8378
Resumen:
Air pollution consists of a wide range of gaseous and particulate pollutants. Exposure to particulate matter (PM) can cause oxidative stress within the lung, which in turn can negatively impact health. The mechanisms by which PM causes oxidative stress include the release of trace metals or organic components from the particle. Previously, we have characterized urban air particles from downtown Buenos Aires (UAP-BA) and, by using in vivo animal studies, found that they are able to generate lung inflammation. Purpose: We studied lung responses to low doses of UAP-BA (15 ìg), with special emphasis on oxidative balance. Methods: We assessed cell viability, total cell number (TCN) and cell differential (CD) on bronchoalveolar lavages (BAL), oxidative metabolism in lung homogenates by tertbutylhydroperoxide-initiated chemiluminescence (CL), thiobarbituric reactive substances (TBARS), total antioxidant potential (TRAP), reduced glutathione (GSH), and apoptosis in lung sections. Results: We found that low UAP-BA exposure increases total cell number, modifies cell differential, and decreases cell viability in the BAL. In lung homogenates, TBARS and CL rose while TRAP and GSH showed no alteration when compared to controls. Occurrence of apoptosis evaluated by TUNEL assay was markedly augmented in UAP-BA exposed animals. Conclusions: Our data further implicate oxidative stress as a possible inducer of apoptosis in lungs from animals exposed to low concentrations of this urban environmental contaminant.in vivo animal studies, found that they are able to generate lung inflammation. Purpose: We studied lung responses to low doses of UAP-BA (15 ìg), with special emphasis on oxidative balance. Methods: We assessed cell viability, total cell number (TCN) and cell differential (CD) on bronchoalveolar lavages (BAL), oxidative metabolism in lung homogenates by tertbutylhydroperoxide-initiated chemiluminescence (CL), thiobarbituric reactive substances (TBARS), total antioxidant potential (TRAP), reduced glutathione (GSH), and apoptosis in lung sections. Results: We found that low UAP-BA exposure increases total cell number, modifies cell differential, and decreases cell viability in the BAL. In lung homogenates, TBARS and CL rose while TRAP and GSH showed no alteration when compared to controls. Occurrence of apoptosis evaluated by TUNEL assay was markedly augmented in UAP-BA exposed animals. Conclusions: Our data further implicate oxidative stress as a possible inducer of apoptosis in lungs from animals exposed to low concentrations of this urban environmental contaminant.