Perfluorodecanoic acid (PFDA) increases oxidative stress through inhibition of mitochondrial β-oxidation

Raimund Widhalm, Sebastian Granitzer, Benjamin Natha, Ottavia Zoboli, Julia Derx, Harald Zeisler, Hans Salzer, Stefan Weiss, Nicole Schmitner, Robin A Kimmel, Tamina Österreicher, Raimund Oberle, Markus Hengstschläger, Martin Distel, Claudia Gundacker

Publikation: Beitrag in Fachzeitschrift (peer-reviewed)Artikel in Fachzeitschrift

Abstract

PER: and polyfluoroalkyl substances (PFAS) are a large group of synthetic organic chemicals that are ubiquitous environmental pollutants. Among PFAS, perfluorodecanoic acid (PFDA) is one of the most toxic compounds, but the molecular basis behind its toxicity is not fully understood. In an interspecies comparison with placental cells (HTR-8/SVneo) and zebrafish embryos, we demonstrate that PFDA induces mitochondrial dysfunction and impairs fatty acid β-oxidation. Reduced β-oxidation leads to less TCA cycle activity, resulting in less NADH and consequently NADPH production. Thereby NADPH-dependent glutathione recycling is impaired, increasing cellular oxidative stress that can only be partially compensated by NRF2 activation.

OriginalspracheEnglisch
Aufsatznummer125595
Seiten (von - bis)125595
FachzeitschriftEnvironmental Pollution
Jahrgang367
DOIs
PublikationsstatusElektronische Veröffentlichung vor Drucklegung - 27 Dez. 2024

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