Decrease in Respiratory Function and Electron Transport Chain Induced by Airborne Particulate Matter (PM10) Exposure in Lung Mitochondria


Por: Delgado-Buenrostro N.L., Freyre-Fonseca V., Cuellar, CMG, Sánchez-Pérez Y., Gutierrez-Cirlos E.B., Cabellos-Avelar T., Orozco-Ibarra M., Pedraza-Chaverri J., Chirino Y.I.

Publicada: 1 jun 2013
Resumen:
Particulate matter, with a mean aerodynamic diameter of =10 µm (PM10), exposure is considered as a risk factor for cardiovascular and respiratory diseases. The mechanism of cell damage induced by PM10 exposure is related to mitochondrial alterations. The aim of this work was to investigate the detailed alterations induced by PM10 on mitochondrial function. Since lung tissue is one of the most important targets of PM10 inhalation, isolated mitochondria from lung rat tissue were exposed to PM10 and structural alterations were analyzed by transmission electron microscopy. Mitochondrial function was evaluated by respiratory control index (RCI), membrane potential, adenosine triphosphate (ATP) synthesis, and activity of respiratory chain. Results showed that exposure to PM10 in isolated mitochondria from lung tissue caused enlarged intermembrane spaces and shape alterations, disruption of cristae, and the decrease in dense granules. Oxygraphic traces showed a concentration-dependent decrease in oxygen consumption and RCI. In addition, mitochondrial membrane potential, ATP synthesis, and activity of complexes II and IV showed an increase and decrease, respectively, after PM10 exposure. PM10 exposure induced disruption in structure and function in isolated mitochondria from lung rat tissue. © 2013, SAGE Publications. All rights reserved.

Filiaciones:
Delgado-Buenrostro N.L.:
 Fac Estudios Super Iztacala, Unidad Biomed, Mexico City, Estado De Mexic, Mexico

Freyre-Fonseca V.:
 Fac Estudios Super Iztacala, Unidad Biomed, Mexico City, Estado De Mexic, Mexico

Sánchez-Pérez Y.:
 Instituto Nacional de Cancerología (INCAN), Subdirección de Investigación Básica, México, D.F, Mexico

Gutierrez-Cirlos E.B.:
 Fac Estudios Super Iztacala, Unidad Biomed, Mexico City, Estado De Mexic, Mexico

Cabellos-Avelar T.:
 Fac Estudios Super Iztacala, Unidad Biomed, Mexico City, Estado De Mexic, Mexico

Orozco-Ibarra M.:
 Laboratorio de Neurobiología Molecular y Celular, INNN-UNAM, Instituto Nacional de Neurología y Neurocirugía, México, D.F, Mexico

Pedraza-Chaverri J.:
 Univ Nacl Autonoma Mexico, Fac Quim, Lab 209, Mexico City 04510, DF, Mexico

Chirino Y.I.:
 Fac Estudios Super Iztacala, Unidad Biomed, Mexico City, Estado De Mexic, Mexico
ISSN: 01926233
Editorial
SAGE PUBLICATIONS INC, 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA, Estados Unidos America
Tipo de documento: Article
Volumen: 41 Número: 4
Páginas: 628-638
WOS Id: 000331464500003
ID de PubMed: 23104767
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