Potential mechanisms of phthalate ester embryotoxicity in the abalone Haliotis diversicolor supertexta

The effects and associated toxicological mechanisms of five phthalate esters (PAEs) on abalone embryonic development were investigated by exposing the embryos to a range of PAEs concentrations (0.05, 0.2, 2 and 10 μg/mL). The results showed that PAEs could significantly reduce embryo hatchability, increase developmental malformations, and suppress the metamorphosis of abalone larvae. The possible toxicological mechanisms of PAEs to abalone embryos included, affecting the Na+–K+-pump and Ca2+–Mg2+-pump activities, altering the peroxidase (POD) level and the malondialdehyde (MDA) production, damaging the extraembryonic membranes structure, as well as disrupting endocrine-related genes (gpx, cyp3a, and 17β-hsd 12) expression properties. Taken together, this work showed that PAEs adversely affected the embryonic ontogeny of abalone. The abilities of PAEs affecting the osmoregulation, inducing oxidative stress, damaging embryo envelope structure, and causing physiological homeostasis disorder, are likely to be a part of the common mechanisms responsible for their embryonic toxicity.

► PAEs affected abalone hatchability, morphogenesis and metamorphosis behavior.
► The toxicity of the five PAEs to embryogenesis was ranked as DBP > DEP > DMP > DOP > DEHP.
► The osmoregulation disorder and oxidative damage are the potential mechanisms.