【摘要】 为评价抗肿瘤药物卡培他滨（CAP）对非靶标生物的毒性,以斑马鱼胚胎为受试生物,研究了CAP对斑马鱼胚胎的发育毒性及对其抗氧化酶系的影响。结果表明,直接暴露于卡培他滨中,造成斑马鱼胚胎死亡率和畸形率增加,且其机能有所下降。当暴露浓度高于20μg·L^-1时,处理后的斑马鱼胚胎死亡率和畸形率显著升高,与对照组相比有极显著差异。CAP浓度为0.2μg·L^-1时,超氧化物歧化酶（SOD）活性和过氧化氢酶（CAT）活性均显著升高,表明机体遭受一定程度的氧化损伤;当浓度高于20μg·L^-1时, SOD和CAT活性显著降低,表明斑马鱼仔鱼所受氧化损伤超出其自我修复能力,引发致死性伤害。本文从发育毒性及氧化应激着手,探究了CAP对非靶标生物的潜在危害,为其生态效应提供一定的科学依据。更多还原

【Abstract】 To investigate the deleterious effects of Capecitabine（CAP） on non-target aquatic organisms, the developmental toxicity of CAP to zebrafish embryos and its effects on the antioxidant enzymes of zebrafish fry were studied. The exposure experiment showed that CAP could cause death and deformity of zebrafish embryos. When the CAP exposure concentration was higher than 20 μg·L^-1, the mortality rate and malformation rate of the treated embryos were significantly higher than those of the control. In antioxidant enzyme activities assays, results revealed that when exposure to 0.2 μg·L^-1 CAP, the superoxide dismutase（SOD） and catalase（CAT） activities in zebrafish fry increased significantly（p < 0.05）, implying that low concentration of CAP could trigger the oxidative stress response of zebrafish. When the CAP concentration was higher than 20 μg·L^-1, the SOD and CAT activities greatly decreased, indicating that the oxidative damage caused by CAP exceeded the restoration capability of zebrafish larvae and caused fatal injuries. In this paper, the developmental toxicity and oxidative stress were used to explore the potential hazards of CAP on the non-target organisms, and to provide a scientific basis for its ecological effects.更多还原