| Objective:Toinvestigatethe effects and the potential mechanism of prenatal DEHP exposure on reproductive systemdevelopment and function of male offspring rats.Method:40 healthypregnant SD rats were randomly divided into 4 groups, including control group(corn oil), 2mg/kg, 10mg/kg and 50 mg/kg DEHP treatment groups, 10 pregnant rats in each group.From G14 to G19, the pregnant rats were treated with different dosage of DEHP by gavage every day. Pregnant rats were weighted from G0 to delivery every morning, and the pregnancy was recorded as well. The body weight and anal genital distance(AGD) of male offspring rat were measured after birth, and then did it every week once. Date of testis descent was confirmed after weaning. Onthe 10 th week after birth, 1 rat per litter and 8 rats per group were randomly selected to be sacrificed by decapitation,whose serumwas separatedfrom the blood and organs including reproductive organs and other major organs were removed. The organs were observed and their coefficient was measured. The rest male rats were fed to the 12 th week.1 rat per litter and 10 rats per group were randomly selected to take part in sexual behavior experiments.Serum testosterone,estradiol,progesterone and luteinizing hormone was analyzed by radioimmunoassay. The mRNA of testis tissue was extractedand then transcripted into cDNA. The cDNA was analyzed by real-time quantitative PCR to test the gene expression level of key enzymes related with testicular steroid hormone synthesis, insulin-like factor 3and peroxisome proliferator-activated receptor γ(PPARγ).Result:1. The appearance of pregnant rats exposed among four groups displayed no abnormity. There was no statistical significance of pregnancy and pregnancy weight gain among groups.2. The average body weight of newborn male rats of 10mg/kg and 50mg/kg exposure group was lower than that of control. The mean AGD of 2mg/kg group was longer than that of control group.3. In10mg/kg and 50mg/kg exposure group, the average time of testis descent were delayed compared with the control group. From first to eighth week after birth, the body weight of 10mg/kg and 50mg/kg exposure group was lower than that of controlgroup. From 9th week to 10 th week after birth, the mean AGD of 10mg/kg and50mg/kg exposure group was shorter than the control. The prostate organ coefficient of group 2mg/kg exposure group was higher than that of control group.4. In 2mg/kg and 50mg/kg exposure group, the male rats mount behavior and ejaculation ability were significantly lower than the control group.5. There were no statistic significant differencesof serumtestosterone, progesterone and luteinizing hormone levels among control and DEHP treatment groups,while theconcentration of estradiol in 50mg/kg group was decreased.Gene expression level of3 beta hydroxylase(3β-HSD) and insulin like-factor 3(insl3) in10mg/kg exposure groupwere significant lower than that of the control group.Conclusion:1. There can be different effects on the weight and AGD of male offspring by prenatal10mg/kg and 50mg/kg DEHP exposure in different stages after birth. The mechanism needs further study.2. Prenatal 2mg/kg DEHP exposure on the growth and development of offspring male rat reproductive system may be related with low-dose effect.3. Prenatal 2mg/kg and 50mg/kg DEHP exposure may influence sexual behavior of offspring male rat, and decrease the ability of mating.4. Prenatal 50mg/kg DEHP exposure may influence serum steroid hormone and decrease estradiol concentration.5. The gene of key enzyme related with steroid hormone synthesisin testis may be reduced after prenatal 10mg/kg DEHP exposure with no significant change of testosterone.It was suggested that the key enzymes related steroid hormone synthesis and insulin-like factor 3 should be detected. |
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