Due
to high viscosity, bitumen extracted from the Alberta oil sands
is diluted with natural gas condensates to form diluted bitumen (dilbit)
to facilitate transport through pipelines. Dilbit that is spilled
into or near a waterbody is subject to environmental weathering processes
such as evaporation and interaction with sediments. This is the first
study that assessed the toxicity of weathered sediment-bound dilbit
(WSD) to fish early life stages. Exposure of zebrafish (Danio rerio) embryos to water-soluble fractions (WSFs)
or water-accommodated fractions (WAFs) of WSD from 30 min to 120 h
postfertilization resulted in pericardial edema, yolk sac edema, and
incidences of uninflated swim bladder. The presence of oil-mineral
aggregates (OMAs) in the WAFs greatly increased toxicity, despite
all fractions having similar concentrations of dissolved polycyclic
aromatic hydrocarbons (PAHs). There were greater cyp1a mRNA abundances in larvae exposed to WAFs, suggesting that there
were differences in bioavailability of PAHs between fractions. However,
there was little evidence that embryotoxicity was caused by oxidative
stress. Results suggest that evaporation and sediment interaction
do not completely attenuate toxicity of dilbit to zebrafish early
life stages, and OMAs in exposures exacerbate toxicity.
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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