Abstract
Lecithotrophic fish embryos rely on finite maternally deposited yolk resources for early development. Toxicant exposure can disrupt the uptake of yolk resources with consequences for development. In this study, we investigate the impacts of altered yolk utilization on fish embryos using the cardiotoxic compound phenanthrene. Zebrafish embryos were exposed to a cardiotoxic concentration of phenanthrene beginning at 6 hpf (hours post-fertilization) until a maximum of 72 hpf. Embryos were stained with Oil Red O to visualize neutral lipids. We then used a nontargeted approach to profile lipids in 24 and 72 hpf embryos after phenanthrene treatment. To assess changes in lipid movement within the embryo, the yolk sac was dissected from the body at 24 and 72 hpf and analyzed separately from the body at 72 hpf. Overall, total metabolites were significantly reduced in the yolk sac, and staining for neutral lipids was reduced in the embryo body at 72 hpf. This result is consistent with significant reductions in triglycerides in both the embryo body and yolk, indicating a limited contribution of impaired cardiac function to lipid mobilization at the dose tested. Additionally, lysophosphatidylcholines and lysophosphatidylethanolamines were significantly increased in the 72 hpf embryo body. Bioinformatic pathway analysis indicated that changes to these lysophospholipids could be linked to a disease model associated with inflammation and neuron demyelination consistent with previously observed injuries to neuronal and eye development in fish embryos and larvae.