Abstract

The aim of the current study was to determine the potential developmental and metabolic abnormalities caused by Cr (VI) exposure on Bufo gargarizans (B. gargarizans) embryos. B. gargarizans embryos were treated with different concentrations of Cr (VI) (13, 52, 104, 208, and 416 μg Cr6+ L−1) for 6 days. Morphological abnormalities, total length, weight and developmental stage were monitored. Malformations of embryos were also examined using scanning electron microscopy (SEM). In addition, the transcript levels of several genes associated with lipid metabolism, oxidative stress, and thyroid hormones signaling pathways were also determined. Our results showed a time-dependent inhibitory effect of Cr (VI) on the growth and development of B. gargarizans embryos. On day 4, total length, weight, and developmental stage were significantly lower at 416 μg Cr6+ L−1 relative to control embryos. On day 6, significant reductions in total length, weight, and developmental stage were observed at 104, 208, and 416 μg Cr6+ L−1. Malformed embryos were found in all Cr (VI) treatments, which were characterized by axial flexures, yolk sac edema and rupture, surface tissue hyperplasia, stunted growth, wavy fin and fin flexure. RT-qPCR results showed that exposure to Cr (VI) down-regulated TRβ and Dio2 mRNA expression and up-regulated Dio3 mRNA level at 416 μg Cr6+ L−1. The transcript levels of SOD and GPx were upregulated at 52, 208, and 416 μg Cr6+ L−1, while the transcript level of HSP90 was downregulated at 52, 208, and 416 μg Cr6+ L−1. Also, mRNA expression of lipid synthesis-related genes (FAE and ACC) were significantly downregulated in embryos treated with 208 and 416 μg Cr6+ L−1, but mRNA expression of fatty acid β-oxidation-related genes (ACOX, CPT, and SCP) was significantly upregulated at 416 μg Cr6+ L−1. Therefore, our results suggested that Cr (VI) could disrupt thyroid endocrine pathways and lipid synthesis, leading to the inhibition of growth and development in B. gargarizans embryos. Furthermore, the decreased ability of scavenging ROS induced by Cr (VI) might be responsible for the teratogenic effects of Cr (VI).

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