氧化石墨烯和多环芳烃复合暴露诱导成年斑马鱼脑组织毒性及其代谢研究

Toxicity and metabolism of adult zebrafish brain tissue induced by combined exposure to graphene oxide and polycyclic aromatic hydrocarbons

为研究氧化石墨烯(Graphene oxide,GO)和多环芳烃(Polycyclic aromatic hydrocarbons,PAHs)共暴露诱发的水生生态毒性效应及相关代谢机理,使用成年斑马鱼为动物模型,研究不同浓度GO(0.01、0.1 mg·L^(-1))、PAHs(含16种优控PAHs,每种PAHs的浓度均为5μg·L^(-1))单独暴露,以及相应浓度的GO-PAHs复合暴露21 d对成年斑马鱼脑组织的毒性及代谢的影响。斑马鱼脑组织酶响应结果表明,0.1 mg·L^(-1) GO和0.1 mg·L^(-1) GO-PAHs处理会显著(P<0.05)降低多环芳烃受体活性,除PAHs组外,其他处理组细胞色素P4501A1(CYP1A1)酶的含量均显著降低。代谢组学分析结果表明,0.1 mg·L^(-1) GO组和0.1 mg·L^(-1) GO-PAHs复合暴露组均会对斑马鱼脑组织的氨基酸和脂肪酸代谢产生显著影响。此外,与GO和PAHs单独暴露组相比,GO-PAHs复合暴露组的酶响应和诱导产生的代谢物水平与GO处理组更相近,说明GO和PAHs复合暴露时,GO在成年斑马鱼脑组织中的代谢毒性效应占主导。

With the increase of application and research on graphene oxide(GO),the risk possibility of its release into the environment has increased,where it may interact with polycyclic aromatic hydrocarbons(PAHs).However,the effects of GO and PAH co-exposure on aquatic ecotoxicity and related metabolic mechanisms are still largely unknown.In this work,adult zebrafish was chosen as a model organism to investigate the toxic effects of single exposure to different concentrations of GO(0.01 mg·L^(-1) and 0.1 mg·L^(-1))and PAHs(including 16 kinds of optimal control PAHs,each with a concentration of 5μg·L^(-1)),and combined exposure to GO-PAHs at the corresponding concentration for 21 days on adult zebrafish brain tissues and the metabolism in these tissues.Enzyme results showed that 0.1 mg·L^(-1) GO and 0.1 mg·L^(-1) GO-PAHs could significantly(P<0.05)decrease aromatic hydrocarbon receptor activity,and that all the treatments(except for PAHs)decreased concentration of cytochrome P4501A1 in adult zebrafish brain tissue.Metabolomics analysis results showed that 0.1 mg·L^(-1) GO,and 0.1 mg·L^(-1) GO-PAHs exposure groups significantly influenced amino acids and fatty acids levels in adult zebrafish brain tissue.Moreover,when compared with the GO and PAHs exposure groups,the enzyme response and metabolite levels induced by the GO-PAHS combined exposure were found to be close to those induced by the GO treatment,revealing that GO was dominant in inducing metabolic toxicity in brain tissue during combined exposure of GO and PAHs in adult zebrafish.