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학술저널
저자정보
김세아 (경북대학교) 이호열 (경북대학교) 박성미 (경북대학교) 김미진 (경북대학교) 이유미 (경북대학교) 윤영란 (경북대학교) 이현경 (한양대학교) 문효방 (한양대학교) 이인규 (경북대학교) 이덕희 (경북대학교)
저널정보
대한당뇨병학회 Diabetes and Metabolism Journal Diabetes and Metabolism Journal Vol.46 No.4
발행연도
2022.7
수록면
592 - 604 (13page)
DOI
10.4093/dmj.2021.0132

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Background: Chronic exposure to low-dose persistent organic pollutants (POPs) can induce mitochondrial dysfunction. This study evaluated the association between serum POP concentrations and oxygen consumption rate (OCR) as a marker of mitochondrial function in humans and <i>in vitro</i> cells.Methods: Serum concentrations of organochlorine pesticides (OCPs) and polychlorinated biphenyls (PCBs) were measured in 323 adults. The OCRs of platelets and peripheral blood mononuclear cells (PBMCs) were assessed in 20 mL of fresh blood using a Seahorse XF analyzer. Additionally, the <i>in vitro</i> effects of Arochlor-1254, β-hexachlorocyclohexane, and p,p´-dichlorodiphenyltrichloroethane at concentrations of 0.1 pM to 100 nM were evaluated in human platelets, human PBMCs, and Jurkat T-cells.Results: The association between serum POP concentrations and OCR differed depending on the cell type. As serum OCP concentrations increased, basal platelet OCR levels decreased significantly; according to the OCP quintiles of summary measure, they were 8.6, 9.6, 8.2, 8.0, and 7.1 pmol/min/μg (<i>P</i> trend=0.005). Notably, the basal PBMC OCR levels decreased remarkably as the serum PCB concentration increased. PBMC OCR levels were 46.5, 34.3, 29.1, 16.5, and 13.1 pmol/min/μg according to the PCB quintiles of summary measure (<i>P</i> trend <0.001), and this inverse association was consistently observed in all subgroups stratified by age, sex, obesity, type 2 diabetes mellitus, and hypertension, respectively. In vitro experimental studies have also demonstrated that chronic exposure to low-dose POPs could decrease OCR levels.Conclusion: The findings from human and <i>in vitro</i> studies suggest that chronic exposure to low-dose POPs can induce mitochondrial dysfunction by impairing oxidative phosphorylation.

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