This paper aims to evaluate the individual and joint toxicities of cadmium sulfate （CdSO4） and α-naphthoflavone （ANF） in zebrafish embryos. As a result, CdSO4 caused both lethal and sub-lethal effects, such as 24...This paper aims to evaluate the individual and joint toxicities of cadmium sulfate （CdSO4） and α-naphthoflavone （ANF） in zebrafish embryos. As a result, CdSO4 caused both lethal and sub-lethal effects, such as 24 h post-fertilization （hpf） death and 72 hpf delayed hatching. However, ANF only caused sub-lethal effects, including 48 hpf cardiac edema and 72 hpf delayed hatching. Taking 24 hpf death and 48 hpf cardiac edema as endpoints, the toxicities of CdSO4 and ANF were significantly enhanced by each other. Consistently, both CdSO4 and ANF caused significant oxidative stress, including decreases in the reduced glutathione （GSH） level, inhibition of superoxide dis- mutase （SOD） activity, as well as increases in malondialdehyde （MDA） content in zebrafish embryos, but these mixtures produced much more significant alterations on the biomarkers. Co-treatment of CdSO4 and ANF significantly down-regulated the mRNA level of multidrug resistance-associated protein （mrp） 1 and cytochrome P450 （cyp） la, which constituted the protective mechanisms for zebraflsh embryos to chemical toxins. In conclusion, co-treatment of CdSO4 and ANF exhibited a much more severe damage in zebraflsh embryos than individual treatment. Meanwhile, production of oxidative stress and altered expression of mrpl and cypla could be important components of such joint toxicity.展开更多
基金Project supported by the National Natural Science Foundation of China （No. 21307154）
文摘This paper aims to evaluate the individual and joint toxicities of cadmium sulfate （CdSO4） and α-naphthoflavone （ANF） in zebrafish embryos. As a result, CdSO4 caused both lethal and sub-lethal effects, such as 24 h post-fertilization （hpf） death and 72 hpf delayed hatching. However, ANF only caused sub-lethal effects, including 48 hpf cardiac edema and 72 hpf delayed hatching. Taking 24 hpf death and 48 hpf cardiac edema as endpoints, the toxicities of CdSO4 and ANF were significantly enhanced by each other. Consistently, both CdSO4 and ANF caused significant oxidative stress, including decreases in the reduced glutathione （GSH） level, inhibition of superoxide dis- mutase （SOD） activity, as well as increases in malondialdehyde （MDA） content in zebrafish embryos, but these mixtures produced much more significant alterations on the biomarkers. Co-treatment of CdSO4 and ANF significantly down-regulated the mRNA level of multidrug resistance-associated protein （mrp） 1 and cytochrome P450 （cyp） la, which constituted the protective mechanisms for zebraflsh embryos to chemical toxins. In conclusion, co-treatment of CdSO4 and ANF exhibited a much more severe damage in zebraflsh embryos than individual treatment. Meanwhile, production of oxidative stress and altered expression of mrpl and cypla could be important components of such joint toxicity.
