Abstract

Exposure to air pollution leads to adverse pulmonary and systemic vascular effects. High levels of plasma HDL cholesterol reduce cardiovascular risk. We explored whether HDL could protect against the prooxidative effects of an organic extract of diesel exhaust particles (DEP) in vascular cells. We used a cell-free fluorescent assay to evaluate DEP oxidation by air, estimated by the degree of Dichlorofluorescein (DCF) fluorescence and tested the ability of HDL to inhibit it. We also evaluated DEP prooxidative effects in bovine aortic endothelial cells and RAW264.7 macrophages by DCF fluorescence. DEP oxidation and prooxidative cellular effects occurred in concentration- and time-dependent manners. Normal HDL inhibited DEP oxidation and prooxidative cellular effects while dysfunctional HDL failed to inhibit DEP oxidation and instead, it promoted further oxidation. In conclusion, DEP prooxidative effects in endothelial cells and macrophages are inhibited by normal HDL. Therefore, HDL may protect against air pollution-mediated adverse vascular effects.

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