| Di(2-ethylhexyl)phthalate(DEHP)is a plasticiser that is widely used in the plastics manufacturing industry.However,with the popularity of plastic products and variations of environmental conditions,DEHP is inevitably emitted into the environment.Aquatic environment became the main environmental medium where DEHP contamination occurs,which poses a potential hazard to human health and safety of aquatic ecology.Therefore,it is of great significance to study the toxicity of DEHP to amphibians in different life cycles.In this study,the ecotoxic effects of DEHP on the embryonic and adult stages of Xenopus tropicalis were investigated by morphology,biochemistry,histopathology,molecular biology and transcriptomics.In this study,the developmental toxicity of DEHP on Xenopus tropicalis embryos were firstly investigated and showed that hatching rate was unaffected but the survival rate was significantly suppressed.Embryonic malformations were firstly observed after 48 h exposure and included pericardial oedema and spinal curvature.However,only the teratogenic rate of pericardial oedema had a dose-effect and a time-effect.Embryonic heart rate increased significantly after 48 h exposure and then decreased progressively with increasing DEHP concentrations.There was a significant decrease in heart area.After 24 h and 96 h exposure,DEHP at concentrations of 1,5 and 10 mg/L significantly inhibited CAT enzyme activity in the heart and significantly inhibited the expression of the corresponding antioxidant gene(cat);heart-related growth genes(nkx2.5)and energy supply genes(ppar?,pgc-1?).These results suggest that the earliest sensitive time point for DEHP to Xenopus tropicalis embryos is 24-48h.Secondly,this study investigated the hepatotoxicity and the potential mechanisms of DEHP on adult Xenopus tropicalis.The results showed that DEHP at a concentration of 1.8mg/L significantly increased the hepatosomatic index and induced structural damage to hepatocytes,including cell vacuolization,deepening of nuclei,morphological abnormality of mitochondria and accumulation of lipids.The area of lipid accumulation also showed a dose-effect relationship.Excessive ROS and suppressed antioxidant genes(nrf2,gst)led to a decreasing in the activity of antioxidants(SOD,CAT,GST,GSH)with increasing DEHP concentrations.In addition,DEHP significantly inhibited gene of lipid metabolism,leading to disruption of intracellular fatty acid metabolism.Change in gene expression was possibly the mechanism for lipid accumulation.Finally,this study investigated the cardiotoxicity and potential mechanisms of DEHP on adult Xenopus tropicalis.The results showed that both 0.6 and 1.8 mg/L DEHP significantly increased Heart Organ Coefficients;The result of HE staining showed that structural myocardial damages were induced in all DEHP treatments,including greater myocardial width,breakage of myocardial fibre.DEHP at 1.8 mg/L induced disordered orientation of fibre and wavy morphology;All DEHP treatments produced ROS in a dose-effect manner.Transcriptomic results showed that DEHP generally caused changes in the functional processes of cytoplasm,cardiomyocytes and related proteins,and mitochondria-related functions.Abnormal Ca+levels in the cytoplasm may be a potential mechanism for myocardial injury and cardiac ROS accumulation;With a dose-effect manner,the down-regulated expression of genes related to the Glucagon Signalling Pathway was the main trigger for the increase in the type of myocardial injury.The above results have improved the aquatic ecotoxicity assessment of DEHP and provided reference information for the regulatory measures and risk systems for plasticizers. |
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