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目的 用邻苯二甲酸二丁酯 (DBP)诱导建立尿道下裂大鼠模型并在分子水平研究其导致尿道下裂的作用机制。方法 将孕鼠在怀孕第 12～ 19天用DBP(5 0 0mg/kg体重 )连续每天灌胃建立仔代雄鼠尿道下裂模型 ,并将孕鼠在第 19天行破宫产取仔代雄鼠的睾丸组织 ,用逆转录 聚合酶链反应 (RT PCR )的方法检测睾酮合成过程中限速酶细胞色素P45 0胆固醇侧链裂解酶(P45 0scc)、3 β羟基类固醇脱氢酶 (3 β HSD)和细胞色素P45 0 17α 羟化酶 (P45 0c17)的mRNA含量水平 ,与正常对照组进行比较。结果 DBP诱导的尿道下裂组胎鼠睾丸组织中P45 0scc、3 β HSD和P45 0c17的基因表达水平较正常对照组均有不同程度的下降 ,两组间差异比较均有统计学意义(P <0 .0 5 )。结论 DBP通过在性发育期干扰仔代雄鼠睾丸组织中睾酮的生物合成途径 ,降低了睾酮水平 ,导致大鼠出生后尿道下裂的出现。
OBJECTIVE: To establish a rat model of hypospadias induced by dibutyl phthalate (DBP) and investigate the mechanism of hypospadias at the molecular level. Methods Pregnant mice were dosed daily with DBP (500 mg / kg body weight) on the 12th to 19th day of pregnancy to establish the hypospadias model of the offspring. The pregnant rats were sacrificed on the 19th day for rupture of the uterus Male rat testis tissues were assayed by reverse transcription polymerase chain reaction (RT PCR) method to detect the rate-limiting enzyme cytochrome P45 0 cholesterol side chain lyase (P45 0scc), 3 β-hydroxysteroid dehydrogenase (3 β HSD) and cytochrome P45 0 17α hydroxylase (P45 0c17) mRNA levels compared with the normal control group. Results The gene expression levels of P45 0scc, 3 β HSD and P45 0c17 in fetal rat testis induced by DBP were lower than those in normal control group, and the difference was statistically significant between the two groups (P < 0 .0 5). Conclusion DBP can reduce the level of testosterone and lead to the appearance of hypospadias in the rat after birth by interfering with the testosterone biosynthesis pathway in testis tissue of Aberrant male rats during sexual development.