Takeshi Shono1, Yuichi Shima, Tsuyoshi Kondo, Sachiyo Suita. 1. Department of Pediatric Surgery, Reproductive and Developmental Medicine, Graduate School of Medical Sciences, Kyushu University, 812-8582, Fukuoka, Japan. shono@pedsurg.med.kyushu-u.ac.jp
Abstract
PURPOSE: Phthalate esters have been shown to cause undescended testes (UT) in rats. It has been proposed that Leydig insulin-like factor 3 (INSL3) may play an important role in testicular descent. The aim of this study was to investigate the effect of mono-n-butyl phthalate (MBP) on both the INSL3 gene expression and the transabdominal testicular descent in rats. METHODS: On the 19th gestational day, the male fetuses that had been exposed to MBP on the 15th to 18th gestational days were dissected and the degree of testicular ascent was examined. Next, quantitative reverse transcriptase polymerase chain reaction was performed to analyze the testicular INSL3 gene expression. At 60 days of age, the testicular position was recorded in the rest of MBP-treated male offspring. RESULTS: On the 19th gestational day, INSL3 messenger RNA expression was significantly decreased in the MBP-treated testes, and the associated degree of testicular ascent was significantly higher than in the controls. At 60 days of age, 12 (54.5%) of 22 rats had either unilateral or bilateral UT. CONCLUSIONS: Prenatal MBP may inhibit the INSL3 gene expression associated with the transabdominal testicular ascent in fetal rats, thereby causing UT in postnatal offspring.
PURPOSE:Phthalate esters have been shown to cause undescended testes (UT) in rats. It has been proposed that Leydig insulin-like factor 3 (INSL3) may play an important role in testicular descent. The aim of this study was to investigate the effect of mono-n-butyl phthalate (MBP) on both the INSL3 gene expression and the transabdominal testicular descent in rats. METHODS: On the 19th gestational day, the male fetuses that had been exposed to MBP on the 15th to 18th gestational days were dissected and the degree of testicular ascent was examined. Next, quantitative reverse transcriptase polymerase chain reaction was performed to analyze the testicular INSL3 gene expression. At 60 days of age, the testicular position was recorded in the rest of MBP-treated male offspring. RESULTS: On the 19th gestational day, INSL3 messenger RNA expression was significantly decreased in the MBP-treated testes, and the associated degree of testicular ascent was significantly higher than in the controls. At 60 days of age, 12 (54.5%) of 22 rats had either unilateral or bilateral UT. CONCLUSIONS: Prenatal MBP may inhibit the INSL3 gene expression associated with the transabdominal testicular ascent in fetal rats, thereby causing UT in postnatal offspring.
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