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Oleic acid and derivatives affect human endothelial cell mitochondrial function and vasoactive mediator production.
Metadata
Journallipids in health and disease2.906Date
2020 Jun 06
4 months ago
Type
Journal Article
Volume
2020-Jun-06 / 19 : 128
Author
Bass VL 1, 2, Soukup JM 3, Ghio AJ 3, Madden MC 4
Affiliation
  • 2. Current Affiliation: RAI Services Company, Winston-Salem, NC, USA.
  • 3. Clinical Research Branch, Public Health and Integrated Toxicology Division, Center for Public Health and Environmental Assessment, ORD, U.S. Environmental Protection Agency, 104 Mason Farm Rd, Chapel Hill, NC, 27514, USA.
  • 4. Clinical Research Branch, Public Health and Integrated Toxicology Division, Center for Public Health and Environmental Assessment, ORD, U.S. Environmental Protection Agency, 104 Mason Farm Rd, Chapel Hill, NC, 27514, USA. [email protected]
Doi
PMIDMESH
Abstract
BACKGROUND: Inhalation of common air pollutants such as diesel and biodiesel combustion products can induce vascular changes in humans which may contribute to increased mortality and morbidity associated with fine particulate matter exposures. Diesel, biodiesel, and other combustion byproducts contain fatty acid components capable of entering the body through particulate matter inhalation. Fatty acids can also be endogenously released into circulation following a systemic stress response to some inhaled pollutants such as ozone. When in the circulation, bioactive fatty acids may interact with cells lining the blood vessels, potentially inducing endothelial dysfunction. To examine whether fatty acids could potentially be involved in human vascular responses to air pollutants, we determined the effects of fatty acids and derivatives on important vascular cell functions.
METHODS: Human umbilical vein endothelial cells (HUVEC) were exposed in vitro to oleic acid (OA) or OA metabolites for 4-48 h. Cytotoxicity, vasodilator production (by ELISA measurement), mitochondrial function (using Sea Horse assays), and iron metabolism (inferred by ICP-OES measurements) were examined, with standard statistical testing (ANOVA, t-tests) employed.
RESULTS: Dose-dependent cytotoxicity was noted at 24 h, with 12-hydroxy OA more potent than OA. Mitochondrial stress testing showed that 12-hydroxy OA and OA induce mitochondrial dysfunction. Analysis of soluble mediator release from HUVEC showed a dose-dependent increase in prostaglandin F2α, a lipid involved in control of vascular tone, at 24 h (85% above controls) after OA-BSA exposure. RT-PCR analysis revealed OA did not induce changes in gene expression at noncytotoxic concentrations in exposed HUVEC, but 12-OH OA did alter ICAM and COX2 gene expression.
CONCLUSIONS: Together, these data demonstrate that FA may be capable of inducing cytotoxic effects and altering expression of mediators of vascular function following inhalation exposure, and may be implicated in air pollutant-induced deaths and hospitalizations. (267 of max 350 words).
Keywords: Endothelial cell Fatty acids Particulate matter Seahorse assay Vascular response
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Lipids Health Dislipids in health and disease
Metadata
LocationEngland
FromBMC

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