[Frontiers in Bioscience E3, 808-817, June 1, 2011]

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

Yessica D Torres-Ramos1,2, Araceli Montoya-Estrada1, Alberto M Guzman-Grenfell1, Javier Mancilla-Ramirez1, Beatriz Cardenas-Gonzalez3, Salvador Blanco-Jimenez3, Jose D Sepulveda-Sanchez3, Alejandra Ramirez-Venegas4, Juan J Hicks1

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


1. Abstract
2. Introduction
3. Materials and methods
3.1. Collection of particulate matter
3.2. Patients
3.3. Treatment strategy
3.4. Stimuli with PM2.5
3.5. Hydroxyl (HO) radical generation
3.6. Biochemical analysis
3.7. Statistics
4. Results
4.1. Respiratory probes
4.2. Particle characteristics
4.3. Erythrocyte oxidative injury by PM10 free fraction
5. Discussion
6. Conclusion
7. Acknowledgements
8. References


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.