Exposure to the Tire Rubber-Derived Contaminant 6PPD-Quinone Causes Mitochondrial Dysfunction In Vitro

体外 代谢物 虹鳟 细胞毒性 呼吸 毒性 活力测定 线粒体 化学 生物 生物化学 有机化学 解剖 渔业
作者
Hannah Mahoney,Francisco Carlos da Silva,Catherine Roberts,Matthew Schultz,Xiaowen Ji,Alper James Alcaraz,David Montgomery,Summer Selinger,Jonathan K. Challis,John P. Giesy,Lynn P. Weber,David M. Janz,Steve Wiseman,Markus Hecker,Markus Brinkmann
出处
期刊:Environmental Science and Technology Letters [American Chemical Society]
卷期号:9 (9): 765-771 被引量:83
标识
DOI:10.1021/acs.estlett.2c00431
摘要

N-(1,3-Dimethylbutyl)-N′-phenyl-p-phenylenediamine-quinone (6PPD-quinone), a rubber tire oxidation product found in road runoff, is highly and acutely toxic to selected salmonids including coho salmon, brook trout, and rainbow trout but not other fish species and invertebrates studied to date. Sensitive species displayed increased ventilation and gasping, suggesting a possible impact on respiration. Here, adherent cell lines RTL-W1 and RTgill-W1 were exposed to 5–80 μg/L 6PPD-quinone, and cytotoxicity, oxygen consumption rate (OCR), and biotransformation of 6PPD-quinone were measured to assess the ability of 6PPD-quinone to uncouple mitochondrial respiration in vitro. RTL-W1 cells were not sensitive to 6PPD-quinone, and exposure did not result in significant impacts on cytotoxicity or OCR. In contrast, RTgill-W1 cells demonstrated decreased cell viability at 80 μg/L and a 2-fold increase in OCR at 20 μg/L. Effects appear to be partly driven by toxicokinetic differences where incubation of RTL-W1 cells with 6PPD-quinone led to almost quantitative conversion of 6PPD-quinone into a suspected hydroxy-metabolite, which was not observed in RTgill-W1 cells. Exposure studies with primary cultures of rainbow trout gill cells indicated that 6PPD-quinone increased OCR by uncoupling the mitochondrial electron transport chain. Together, these findings suggest that 6PPD-quinone toxicity might be driven by a tissue-specific disruption of mitochondrial respiration.
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