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Effects of maternal exposure to low doses of DES on testicular steroidogenesis and spermatogenesis in male rat offspring.
J Reprod Dev. 2009 Dec; 55(6):629-37.JR

Abstract

Our previous studies have demonstrated that prenatally administered diethylstilbestrol (DES) impairs testicular endocrine function in male offspring. The present study examined whether maternal DES treatment influences testicular steroidogenesis and spermatogenesis. DES was injected subcutaneously at 0.5 or 1.5 microg/kg/day (DES 0.5 and 1.5 groups, respectively) into pregnant SD rats on days 7-21 of gestation. Male offspring in the DES 0.5 and 1.5 groups were autopsied at 1, 3, 6 and 15 weeks after birth. At 1 week, DES treatment did not lead to a change in the volume of P450scc-positive cells (Leydig cells), suggesting that DES has no inhibitory effect on the development of Leydig cells. DES administration disrupted luteinizing hormone receptor (LHr) expression and exerted inhibitory effects on signal transduction from LHr to steroidogenic acute regulatory protein (StAR) in testicular steroidogenesis (P<0.05), although there were no changes in the mRNA expression levels of steroidogenic enzymes, such as P450scc, 3beta-hydroxysteroid dehydrogenase (3beta-HSD) and P450(17 alpha), which may have caused a decrease in the plasma testosterone level. DES treatment did not disrupt the cycle of spermatogenesis but did upregulate the expression levels of androgen receptor (AR) mRNA in both DES groups at 15 weeks (P<0.05). These results indicate that maternal DES treatment disrupts steroidogenesis but induces a high level of AR mRNA expression to counteract the low levels of testosterone during spermatogenesis.

Authors+Show Affiliations

Department of Anatomy II, School of Veterinary Medicine, Azabu University, Kanagawa, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

19734697

Citation

Kobayashi, Tetsuo, et al. "Effects of Maternal Exposure to Low Doses of DES On Testicular Steroidogenesis and Spermatogenesis in Male Rat Offspring." The Journal of Reproduction and Development, vol. 55, no. 6, 2009, pp. 629-37.
Kobayashi T, Shirai M, Sakaue M, et al. Effects of maternal exposure to low doses of DES on testicular steroidogenesis and spermatogenesis in male rat offspring. J Reprod Dev. 2009;55(6):629-37.
Kobayashi, T., Shirai, M., Sakaue, M., Murakami, M., Ochiai, H., Arishima, K., & Yamamoto, M. (2009). Effects of maternal exposure to low doses of DES on testicular steroidogenesis and spermatogenesis in male rat offspring. The Journal of Reproduction and Development, 55(6), 629-37.
Kobayashi T, et al. Effects of Maternal Exposure to Low Doses of DES On Testicular Steroidogenesis and Spermatogenesis in Male Rat Offspring. J Reprod Dev. 2009;55(6):629-37. PubMed PMID: 19734697.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Effects of maternal exposure to low doses of DES on testicular steroidogenesis and spermatogenesis in male rat offspring. AU - Kobayashi,Tetsuo, AU - Shirai,Mitsuyuki, AU - Sakaue,Motoharu, AU - Murakami,Masaru, AU - Ochiai,Hideharu, AU - Arishima,Kazuyoshi, AU - Yamamoto,Masako, Y1 - 2009/09/07/ PY - 2009/9/8/entrez PY - 2009/9/8/pubmed PY - 2010/3/13/medline SP - 629 EP - 37 JF - The Journal of reproduction and development JO - J Reprod Dev VL - 55 IS - 6 N2 - Our previous studies have demonstrated that prenatally administered diethylstilbestrol (DES) impairs testicular endocrine function in male offspring. The present study examined whether maternal DES treatment influences testicular steroidogenesis and spermatogenesis. DES was injected subcutaneously at 0.5 or 1.5 microg/kg/day (DES 0.5 and 1.5 groups, respectively) into pregnant SD rats on days 7-21 of gestation. Male offspring in the DES 0.5 and 1.5 groups were autopsied at 1, 3, 6 and 15 weeks after birth. At 1 week, DES treatment did not lead to a change in the volume of P450scc-positive cells (Leydig cells), suggesting that DES has no inhibitory effect on the development of Leydig cells. DES administration disrupted luteinizing hormone receptor (LHr) expression and exerted inhibitory effects on signal transduction from LHr to steroidogenic acute regulatory protein (StAR) in testicular steroidogenesis (P<0.05), although there were no changes in the mRNA expression levels of steroidogenic enzymes, such as P450scc, 3beta-hydroxysteroid dehydrogenase (3beta-HSD) and P450(17 alpha), which may have caused a decrease in the plasma testosterone level. DES treatment did not disrupt the cycle of spermatogenesis but did upregulate the expression levels of androgen receptor (AR) mRNA in both DES groups at 15 weeks (P<0.05). These results indicate that maternal DES treatment disrupts steroidogenesis but induces a high level of AR mRNA expression to counteract the low levels of testosterone during spermatogenesis. SN - 0916-8818 UR - https://www.unboundmedicine.com/medline/citation/19734697/Effects_of_maternal_exposure_to_low_doses_of_DES_on_testicular_steroidogenesis_and_spermatogenesis_in_male_rat_offspring_ L2 - https://joi.jlc.jst.go.jp/JST.JSTAGE/jrd/20223?from=PubMed DB - PRIME DP - Unbound Medicine ER -