Parental exposure to environmental cadmium causes developmental defects in the rare minnow (Gobiocypris rarus) embryos: The association between ROS-mediated oxidative stress and developmental dysfunction

Cadmium is widely distributed in aquaculture systems. The exposure of parental fish species to cadmium is known to retard of growth and cause death in offspring. However, the potential mechanisms responsible for how parental cadmium exposure effects embryonic development yet to be elucidated. Herein, we investigated the effects of parental cadmium exposure on embryonic developmental abnormalities in rare minnow. Our results demonstrated that significantly increased rates of malformation were recorded in the parental cadmium exposure groups. The most significant impairments and morphological changes were egg condensation and spine curvature malformations. Parental cadmium exposure significantly increased the cadmium content of rare minnow embryos, thus increasing the production of reactive oxygen species (ROS) and malondialdehyde (MDA). Further investigation found that parental cadmium exposure reduced superoxide dismutase (SOD) activity and significantly up-regulated the expression of antioxidative genes (gpx-1, cat and mn-sod) and detoxifying metallothionein (MT) in rare minnow embryos. In addition, stress-related genes (hsp70, ccyp1α and jnk) were significantly upregulated while developmental-related genes (wnt8α, vezf1 and mstn) were significantly downregulated in rare minnow embryos. Our analysis revealed that parental cadmium exposure in rare minnow caused developmental abnormalities in embryos via the accumulation of cadmium content which induced oxidative stress and developmental dysfunction. Collectively, our analysis suggested that environmental cadmium may pose a severe threat to the continuation of certain fish species.