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Particulate Matter Promotes In Vitro Receptor-Recognizable Low-Density Lipoprotein Oxidation and Dysfunction of Lipid Receptors


  • Contract Grant Sponsor: Consejo Nacional de Ciencia y Tecnología.

  • Contract Grant Number: CONACyT-M43138.

  • Contract Grant Sponsor: NIH/NIEHS.

  • Contract Grant Numbers: R01 ES016932-01 and R01 ES017022-01.

Correspondence to: Álvaro R. Osornio-Vargas.


Particulate matter may promote cardiovascular disease, possibly as a consequence of its oxidative potential. Studies using susceptible animals indicate that particulate matter aggravates atherosclerosis by increasing lipid/macrophage content in plaques. Macrophage lipid uptake requires oxidized low-density lipoprotein and scavenger receptors; same receptors are involved in particulate matter uptake. We studied in vitro particulate matter potential to oxidize low-density lipoproteins and subsequent cell uptake through scavenger receptors. Particulate matter-induced low-density lipoproteins oxidation was evaluated by the thiobarbituric acid assay. Binding/internalization was tested in wild type and scavenger receptor–transfected Chinese hamster ovary cells, and in RAW264.7 cells using fluorescently labeled low-density lipoproteins. Dose-dependent binding/internalization only occurred in scavenger receptor–transfected Chinese hamster ovary cells and RAW264.7 cells. Competition binding/internalization using particles showed that particulate matter induced decreased binding (∼50%) and internalization (∼70%) of particle-oxidized low-density lipoproteins and native low-density lipoproteins. Results indicate that particulate matter was capable of oxidizing low-density lipoproteins, favoring macrophage internalization, and also altered scavenger and low-density lipoproteins receptor function. © 2012 Wiley Periodicals, Inc. J BiochemMol Toxicol 27:69-76, 2013; View this article online at DOI 10.1002/jbt.21452