邻苯二甲酸二辛酯对热带爪蛙胚胎发育和心脏毒性效应研究

Toxic effect of di-(2-ethylhexyl) phthalate on development and heart of Xenopus tropicalis embryos

邻苯二甲酸二辛酯(DEHP)是一种增加塑料柔软性的化学物质,容易释放到自然水环境中,因此,DEHP所造成的生态风险值得关注.目前,有关DEHP对两栖类动物胚胎的早期发育和心脏毒性研究仍较少.本研究通过96 h的暴露实验,探究DEHP对热带爪蛙胚胎的早期发育毒性和心脏毒性.结果表明,DEHP虽然不会造成胚胎孵化率的显著变化(p>0.05),但造成了存活率的极显著下降(p<0.01).在DEHP影响下,胚胎产生的畸形类型主要是心包水肿和脊柱弯曲,其中,胚胎的心包水肿率显著高于对照组并且具有剂量-效应和时间-效应关系(p<0.01).在暴露DEHP 24 h后,胚胎的心率剧烈升高,随着暴露时间的增加,心率逐渐降低.0.1、0.5 mg·L^(-1)DEHP能导致胚胎的心脏面积(舒张状态)增大,但随着暴露浓度的增加心脏面积逐渐减小.胚胎心脏抗氧化酶SOD和CAT的活力随着暴露浓度的增加,产生一致的变化趋势.SOD在第48 h和第96 h对DEHP较不敏感,CAT则在第48 h和96 h均被显著抑制(p<0.01).另外,在1、5、10 mg·L^(-1)浓度下,DEHP引发的心包水肿和心率异常下降可能与心脏发育基因nkx2.5、心脏供能基因pparα和pgc-1α显著下调(p<0.05,p<0.01)有关.在暴露过程中,不同的毒性效应最早发生在第48 h,暴露的第48 h是DEHP诱导热带爪蛙胚胎产生心脏毒性的最早时间点.该结果可为评估增塑剂对水生动物胚胎的毒性效应和生态风险提供信息和参考.

Di-(2-ethylhexyl)phthalate(DEHP),a chemical increases the softness of plastics,is easily released into the natural water environment.Therefore,the ecological risk posed by DEHP is worthy of attention. There are relatively few studies on the early development and cardiotoxicity of DEHP on amphibian embryos. In this study,we investigated the early developmental toxicity and cardiotoxicity of DEHP on Xenopus tropicalis embryos through 96-h exposure experiment. The results showed that DEHP did not cause significant changes in embryo hatching rate(p>0.05),but caused a very significant decrease in survival rate(p<0.01). The type of malformations induced by DEHP were pericardial edema and spinal curvature. DEHP significantly induced pericardial edema with a dose and time dependent manners when compared with controls(p<0.01). After 24-h exposure,the heart rate of embryos increased dramatically and decreased gradually with exposure time extension. 0.1 and 0.5 mg·L^(-1)DEHP resulted in an increase in the heart area(diastolic state)of embryos,which decreased gradually with increasing exposure concentration. The activity of antioxidant enzymes superoxide dismutase(SOD)and catalase(CAT)in embryonic hearts showed a consistent trend with increasing exposure concentration. SOD was less sensitive to DEHP at 48 h and 96 h,while CAT was significantly inhibited at 48 h and 96 h(p<0.01). In addition,the pericardial edema and abnormal decrease in heart rate at 1,5,and 10 mg·L^(-1)concentrations may be associated with the significant downregulation(p<0.05,p<0.01)of cardiac development gene(nkx2.5)and the cardiac energy supply genes(pparα and pgc-1α). During exposure,the earliest toxic effects of DEHP were observed after 48-h exposure. The 48th hour of exposure was the earliest time point for cardiotoxicity in Xenopus tropicalis embryos. Taken together,these results may provide information and references for assessing the toxic effects and ecological risks of plasticizers on aquatic animal embryos.