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Journal of Zhejiang University SCIENCE B
ISSN 1673-1581(Print), 1862-1783(Online), Monthly
2014 Vol.15 No.9 P.766-775
Individual and joint toxic effects of cadmium sulfate and α-naphthoflavone on the development of zebrafish embryo
Abstract: 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.
Key words: Joint toxicity, Cadmium sulfate, α-Naphthoflavone, Zebrafish embryo, Oxidative stress
创新要点:首次对硫酸镉与α-萘黄酮的联合毒性进行了研究,并探索了氧化应激、ATP结合盒式(ABC)转运蛋白及细胞色素P450蛋白(CYP)1A在化合物联合毒性中的作用。
研究方法:在不同时间点,依据形态学指标检测硫酸镉与α-萘黄酮单独使用与联合使用时对斑马鱼胚胎的致死与致畸性毒性。取样品,采用试剂盒检测不同处理状态下斑马鱼胚胎中谷胱甘肽(GSH)、超氧化物歧化酶(SOD)及丙二醛(MDA)三个氧化还原指标的改变,聚合酶链式反应(PCR)检测样品中多药耐药蛋白(mrp)1及cyp1a基因表达水平的改变。
重要结论:硫酸镉与α-萘黄酮的联用能够产生远大于个体且显著增强各自的毒性,而这种增强作用机理在于氧化应激压力的产生,以及两者合用下mrp1及cyp1a基因表达水平的改变。
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DOI:
10.1631/jzus.B1400091
CLC number:
Q89
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On-line Access:
2024-08-27
Received:
2023-10-17
Revision Accepted:
2024-05-08
Crosschecked:
2014-08-15