IMR Press / FBE / Volume 3 / Issue 3 / DOI: 10.2741/E288

Frontiers in Bioscience-Elite (FBE) is published by IMR Press from Volume 13 Issue 2 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Article

Urban PM2.5 induces ROS generation and RBC damage in COPD patients

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1 Departamento de Bioquimica y Biologia Molecular, Instituto Nacional de Perinatologia. Isidro Espinosa de los Reyes (INPerIER), Mexico
2 Escuela Superior de Medicina, Instituto Politecnico Nacional, Mexico
3 Direccion de Investigacion Experimental en Contaminacion Atmosferica, Centro Nacional de Investigacion y Capacitacion Ambiental, Instituto Nacional de Ecologia, Mexico
4 Clinica de Tabaquismo, Instituto Nacional de Enfermedades Respiratorias (INER), Ismael Cosio Villegas, Mexico

*Author to whom correspondence should be addressed.

Front. Biosci. (Elite Ed) 2011, 3(3), 808–817; https://doi.org/10.2741/E288
Published: 1 June 2011
Abstract

Particulate matters (PM) produce adverse effects on the respiratory system and cause COPD. These effects are thought to involve intrinsic generation of ROS which are present in ambient PM (transition metals and aromatic organic compounds). Here, we examined the chemical composition and ultra-microscopic structure of PM2.5. The effect of this PM was studied in red blood cell (RBC) membranes (ghosts) from healthy volunteers (n = 11) and COPD patients (n = 43). These effects were compared with that produced by a Fenton metal-catalytic ROS generator. Oxidative biomarkers and cell damage were singificantly increased in presence of PM2.5 or ROS generator in RBC of COPD patients as compared with those in cells from healthy volunteers. In contrast, total SH groups, band 3 phospho-tyrosine phosphatase (PTPase) and glucose-6 phosphate dehydrogenase (G6PD) activities were all diminished in cells from COPD patients. In conclusion, PM2.5 increases damage to RBCs from COPD patients, decreases the activity of PTPase and G6PD, and alters the function of the anionic exchanger (AE1) and the antioxidant response by decreasing SH groups.

Keywords
Tissue
Hypoxia
COPD
Oxidative Stress
Erythrocyte
Anionic Exchanger
Glucose 6 Phosphate Dehydrogenase
Free Radicals
Phosphotyrosine Phosphatase
PM
Particulate matter
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