Study On The Mechanism Of DEHP-Induced Testicular Toxicity In Quails

Di(2-ethylhexyl)phthalate(DEHP)is an environmental endocrine disruptor,which widely exists in the atmosphere,water and soil,thus threatening human and animal health and affecting ecosystem balance.In addition to neurotoxicity,immunotoxicity and endocrine toxicity,DEHP has a particularly significant effect on reproductive system.However,the mechanism of DEHP-induced male reproductive toxicity remains unclear in poultry.In this study,male quails were given DEHP by gavage continuously.The clinical symptoms and histopathological changes of testes were observed.Sperm quality,serum biochemical function,antioxidant enzyme function,nuclear receptor response,CYP450 homeostasis,serum hormone level and expression of sex hormone related genes in hypothalamus-pituitary-testis axis(HPTA)were also detected.The results showed that:(1)DEHP exposure changed blood biochemistry,which increased cardiac function-related indicators(CK and LDH),renal function-related indicators(Cre and UA).In addition,DEHP caused abnormal liver function related indicators(AST,ALT,AST/ALT,TBIl,DBIl and TP).Therefore,DEHP caused biochemical damage.Histopathological observation showed that the chromatin in testicular germ cells contracted,the spermatogenic cells arranged irregularly,and the lumen of seminiferous tubules narrowed.Sperm motility and sperm viability decreased.It is suggested that DEHP exposure can cause testicular dysplasia.(2)DEHP exposure induced the decrease of T-AOC,GST and T-SOD,and the increase of MDA content in testicular tissues,which can induce oxidative stress in testicular tissues of quail,and further made damage to quail testicular tissues.(3)DEHP exposure induced the increase of CYP450 content and abnormal enzyme activity,the increase of nuclear receptor(AHR,CAR and PXR)gene expression and the increase of CYPs related gene expression.It is suggested that DEHP exposure can cause CYP450 s homeostasis by interfering with nuclear receptor response,which should be one of the mechanisms of testicular toxicity of DEHP and its metabolites.(4)DEHP exposure resulted in changes in sex hormone content,disorders in the expression of sex hormone-related genes and proteins,abnormal regulation of HPTA,and testosterone synthesis disorder.It is suggested that DEHP exposure can interfere with the regulation of HPTA,which should be one of the mechanisms of testicular dysplasia caused by DEHP.In conclusion,DEHP exposure causes biochemical damage and oxidative stress,and induces CYP450 s homeostasis by interfering with nuclear receptor response,thus exerting testicular toxicity.And DEHP exposure interfered with the regulation of HPTA,caused testosterone synthesis disorder,affected spermatogenesis,and further caused testicular dysplasia,which has a serious toxic effect on the male reproductive system of quails.