Parental exposure to CdSe/ZnS QDs affects cartilage development in rare minnow (Gobiocypris rarus) offspring

Cartilage development is a sensitive process that is easily disturbed by environmental toxins. In this study, the toxicity of CdSe/ZnS quantum dots on the skeleton of the next generation (F1) was evaluated using rare minnows (Gobiocypris rarus) as model animals. Four-month-old sexually mature parental rare minnows (F0) were selected and treated with 0, 100, 200, 400 and 800 nmol/L CdSe/ZnS quantum dots for 4 days. Embryos of F1 generation rare minnows were obtained by artificial insemination. The results showed that with increasing maternal quantum dots exposure, the body length of F1 embryos decreased, the overall calcium content decreased, and the deformity and mortality rates increased. Alcian blue staining results showed that the lengths of the craniofacial mandible, mandibular arch length, mandibular width, and CH-CH and CH-PQ angles of larvae of rare minnows increased; histological hematoxylin-eosin staining further indicated that quantum dots affected the development of chondrocytes. Furthermore, high concentrations of CdSe/ZnS quantum dots inhibited the transcript expression of the bmp2b, bmp4, bmp6, runx2b, sox9a, lox1 and col2 alpha 1 genes. In conclusion, CdSe/ZnS quantum dots can affect the skeletal development of F1 generation embryos of rare minnows at both the individual and molecular levels, the damage to the craniofacial bone is more obvious, and the toxic effect of high concentrations of quantum dots (400 nmol/L and 800 nmol/L) is more significant.

Automated summary

This study evaluated the toxicity of CdSe/ZnS quantum dots on the skeletal development of the rare minnows' next generation using rare minnows as model animals. The results showed that maternal exposure to quantum dots led to decreased body length, overall calcium content, and increased deformity and mortality rates in the F1 embryos. The quantum dots also affected the craniofacial bone and inhibited the expression of several genes.