Oxidative stress and apoptosis are induced in human endothelial cells exposed to urban particulate matter

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• 作者：Angé ; lica Montiel-Dá ; valos ; Mar&#xed ; a de Jesú ; s Ibarra-Sá ; nchez ; José ; Luis Ventura-Gallegos ; Ernesto Alfaro-Moreno ; Rebeca Ló ; pez-Marure
• 关键词：Particulate matter ; TNF-α ; Endothelial cells ; NF-κ ; B ; Inflammation ; Oxidative stress
• 刊名：Toxicology in Vitro
• 出版年：2010
• 出版时间：February 2010
• 年：2010
• 卷：24
• 期：1
• 页码：135-141
• 全文大小：624 K

文摘

Correlations between exposure to particle matter (PM) with an aerodynamic diameter  2.5 or 10 μm (PM_2.5 and PM₁₀, respectively) with cardiovascular effects have been demonstrated recently. Endothelial cells seem to play a relevant role in the responses to PM due to their participation in pro-inflammatory events. In this study we determined the effect of PM_2.5 and PM₁₀ from Mexico City on human endothelial cells by means of evaluating reactive oxygen species (ROS), nitric oxide (NO), NF-κB translocation and cell death. For this purpose we used human umbilical vein endothelial cells (HUVEC) as a model.

The production of ROS was determined by the reduction of H₂DCFDA and NO by Griess reagent. The translocation of NF-κB was evaluated by Electrophoretic Mobility Shift Assay (EMSA) and the cellular death by the translocation of phosphatidylserine. TNF-α was used as a positive control for endothelial cell activation.

PM_2.5 and PM₁₀ induced the production of ROS (77 % and 126 % increase, respectively, vs. control) and NO (up to 132 % and 233 % increase, respectively, vs. control). PM_2.5 and PM₁₀ also induced the nuclear translocation of NF-κB. All these events were associated with apoptosis. In conclusion, the activation of HUVEC induced by PM_2.5 and PM₁₀ is related with an oxidative stress, suggesting that these particles may participate in the development of cardiovascular and inflammatory diseases.