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
目的研究硫酸镉诱导人胚胎肝(L-02)细胞热应激蛋白70(heat shock protein 70,HSP70)表达及氧化应激作用,以探讨HSP70表达与细胞抗氧化作用的关系。方法将对数生长期的L-02细胞分别暴露于终浓度为0(对照,双蒸水)、1、2、4、8、16、32、64...目的研究硫酸镉诱导人胚胎肝(L-02)细胞热应激蛋白70(heat shock protein 70,HSP70)表达及氧化应激作用,以探讨HSP70表达与细胞抗氧化作用的关系。方法将对数生长期的L-02细胞分别暴露于终浓度为0(对照,双蒸水)、1、2、4、8、16、32、64、128μmol/L的硫酸镉溶液培养24h,采用MTT法测定细胞活性。将对数生长期的L-02细胞分别暴露于含终浓度为0(对照,双蒸水)、1、2、4μmol/L硫酸镉的培养基中,培养24h后,检测细胞裂解液中谷胱甘肽过氧化物酶(GSH-Px)活力、超氧化物歧化酶(SOD)的活力和丙二醛(MDA)的含量以及细胞HSP70的表达。结果与对照组比较,2~128μmol/L硫酸镉染毒组L-02细胞的存活率降低,差异有统计学意义(P<0.05);且随着硫酸镉染毒浓度的升高,L-02细胞的存活率呈下降趋势明显。与对照组比较,4μmol/L硫酸镉染毒组L-02细胞SOD、GSH-Px活力均上升,差异有统计学意义(P<0.05);而各浓度硫酸镉染毒组L-02细胞内MDA的含量均无明显变化。随着硫酸镉染毒浓度的升高,L-02细胞内HSP70蛋白的阳性表达呈上升趋势。结论在本研究剂量下,硫酸镉可诱导L-02细胞株HSP70表达上调,引起细胞抗氧化活性增强。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.
文摘目的研究硫酸镉诱导人胚胎肝(L-02)细胞热应激蛋白70(heat shock protein 70,HSP70)表达及氧化应激作用,以探讨HSP70表达与细胞抗氧化作用的关系。方法将对数生长期的L-02细胞分别暴露于终浓度为0(对照,双蒸水)、1、2、4、8、16、32、64、128μmol/L的硫酸镉溶液培养24h,采用MTT法测定细胞活性。将对数生长期的L-02细胞分别暴露于含终浓度为0(对照,双蒸水)、1、2、4μmol/L硫酸镉的培养基中,培养24h后,检测细胞裂解液中谷胱甘肽过氧化物酶(GSH-Px)活力、超氧化物歧化酶(SOD)的活力和丙二醛(MDA)的含量以及细胞HSP70的表达。结果与对照组比较,2~128μmol/L硫酸镉染毒组L-02细胞的存活率降低,差异有统计学意义(P<0.05);且随着硫酸镉染毒浓度的升高,L-02细胞的存活率呈下降趋势明显。与对照组比较,4μmol/L硫酸镉染毒组L-02细胞SOD、GSH-Px活力均上升,差异有统计学意义(P<0.05);而各浓度硫酸镉染毒组L-02细胞内MDA的含量均无明显变化。随着硫酸镉染毒浓度的升高,L-02细胞内HSP70蛋白的阳性表达呈上升趋势。结论在本研究剂量下,硫酸镉可诱导L-02细胞株HSP70表达上调,引起细胞抗氧化活性增强。
