Individual and joint toxic effects of cadmium sulfate and α-naphthoflavone on the development of zebrafish embryo
Individual and joint toxic effects of cadmium sulfate and α-naphthoflavone on the development of zebrafish embryo
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DOI：
10.1631/jzus.b1400091
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发表时间：
2014-09
影响因子：
5.1
通讯作者：
Jian Yin;Jian-ming Yang;Feng Zhang;Peng Miao;Yingxin Lin;Mingli Chen
中科院分区：
文献类型：
--
作者：
Jian Yin;Jian-ming Yang;Feng Zhang;Peng Miao;Yingxin Lin;Mingli Chen
研究了硫酸镉（CdSO 4）和α-萘甲酮（ANF）对斑马鱼胚胎的个体毒性和联合毒性。结果表明，CdSO 4可引起受精后24 h死亡和72 h孵化延迟等致死和亚致死效应。然而，ANF仅引起亚致死效应，包括48 hpf心脏水肿和72 hpf延迟孵化。以24 hpf死亡和48 hpf心脏水肿为终点，CdSO 4和ANF的毒性相互增强。结果表明，CdSO 4和ANF均能引起斑马鱼胚胎氧化应激，包括还原型谷胱甘肽（GSH）水平降低、超氧化物歧化酶（SOD）活性抑制和丙二醛（MDA）含量升高，但二者的混合物对生物标志物的影响更为显著。CdSO 4和ANF联合处理显著下调斑马鱼胚胎多药耐药相关蛋白（mrp）1和细胞色素P450（cyp）1a的mRNA水平，这可能是斑马鱼胚胎对化学毒素的保护机制。总之，CdSO 4和ANF联合处理对斑马鱼胚胎的损伤比单独处理严重得多。同时，氧化应激的产生和mrp 1和cyp 1a表达的改变可能是这种联合毒性的重要组成部分。
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 dismutase (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) 1a, which constituted the protective mechanisms for zebrafish embryos to chemical toxins. In conclusion, co-treatment of CdSO4 and ANF exhibited a much more severe damage in zebrafish embryos than individual treatment. Meanwhile, production of oxidative stress and altered expression of mrp1 and cyp1a could be important components of such joint toxicity.