N-(1,3-Dimethylbutyl)-N′-phenyl-p-phenylenediamine-quinone (6PPD-quinone), a transformation product of the rubber tire antioxidant 6PPD, has recently been identified as the chemical responsible for urban runoff mortality syndrome in coho salmon, with a median lethal concentration (LC50) of <0.1 μg/L. Subsequent studies have failed to confirm comparable sensitivity in other fish species. Here, we investigated the acute toxicity of 6PPD-quinone to rainbow trout, brook trout, Arctic char, and white sturgeon. Fish were exposed under static renewal conditions, and exposure concentrations were verified analytically. Mortalities in brook trout occurred between 1.2 and 20 h, while mortalities began after 7 h and spanned 60 h in rainbow trout. The LC50s in brook trout (24 h) and rainbow trout (72 h) were 0.59 and 1.00 μg/L, respectively. Both species showed characteristic symptoms (increased ventilation, gasping, spiraling, and loss of equilibrium) shortly before death. No mortalities were observed after exposure of either char or sturgeon for 96 h at measured concentrations as high as 14.2 μg/L. This is the first study to demonstrate the acute toxicity of 6PPD-quinone to other fishes of commercial, cultural, and ecological importance at environmentally relevant concentrations and provides urgently needed information for environmental risk assessments of this contaminant of emerging concern.

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Oogenesis is the process by which a primary oocyte develops into a fertilizable oocyte, making it critical to successful reproduction in fish. In zebrafish (Danio rerio), there are five stages of oogenesis. During the final step (oocyte maturation), the maturation-inducing hormone 17α,20β-dihydroxy-4-pregnen-3-one (MIH) activates the membrane progestin receptor, inducing germinal vesicle breakdown. Using in vitro assays, it has been shown that anthropogenic stressors can dysregulate MIH-induced oocyte maturation. However, it is unknown whether the in vitro assay is predictive of reproductive performance after in vivo exposure. We demonstrate that a known inhibitor of oocyte maturation, malathion, and a structurally related chemical, dimethoate, inhibit oocyte maturation. However, malaoxon and omethoate, which are metabolites of malathion and dimethoate, did not inhibit oocyte maturation. Malathion and dimethoate inhibited maturation to a similar magnitude when oocytes were exposed for 4 h in vitro or 10 days in vivo, suggesting that the in vitro zebrafish oocyte maturation assay might be predictive of alterations to reproductive performance. However, when adult zebrafish were exposed to malathion for 21 days, there was no alteration in fecundity or fertility in comparison with control fish. Our study supports the oocyte maturation assay as being predictive of the success of in vitro oocyte maturation after in vivo exposure, but it remains unclear whether inhibition of MIH-induced oocyte maturation in vitro correlates to decreases in reproductive performance.

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