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Toxicogenomic difference between diethylstilbestrol and 17β‐estradiol in mouse testicular gene expression by neonatal exposure
Author(s) -
Adachi Tetsuya,
Koh KyuBom,
Tainaka Hitoshi,
Matsuno Yoshiharu,
Ono Yushin,
Sakurai Kenichi,
Fukata Hideki,
Iguchi Taisen,
Komiyama Masatoshi,
Mori Chisato
Publication year - 2004
Publication title -
molecular reproduction and development
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.745
H-Index - 105
eISSN - 1098-2795
pISSN - 1040-452X
DOI - 10.1002/mrd.20004
Subject(s) - biology , diethylstilbestrol , gene expression , andrology , estrogen , gene , real time polymerase chain reaction , microarray analysis techniques , medicine , endocrinology , gene expression profiling , microarray , complementary dna , reverse transcription polymerase chain reaction , spermatogenesis , genetics
In this study, we investigated the effects of neonatal exposure to exogenous estrogen (diethylstilbestrol: DES, 17β‐estradiol: E 2 ) on testicular gene expressions. Male C57BL/6J mice, 1 day after birth, were subcutaneously injected with DES or E 2 (3 μg/mouse/day) for 5 days, and then they were raised for 8 weeks. In morphological observation of 8‐week‐old mice testes, spermatozoa were absent from many seminiferous tubules in DES‐treated mice testes, but there was no change in E 2 ‐treated mice testes. Analysis of in‐house cDNA microarray (mouse cDNA 889 genes) revealed that 17 genes were altered in DES‐treated mice testes at 8 weeks of age, compared to each control. Real‐time reverse transcription‐polymerase chain reaction (real‐time RT‐PCR) analysis of these genes revealed that some genes, which were changed in E 2 ‐treated testis, were the same as in DES‐treated testis, whereas in other cases there was a difference between DES‐treated and E 2 ‐treated testis. The present results suggest that each exogenous estrogenic compound has both a common gene expression change pattern and its own testicular gene expression change pattern. Mol. Reprod. Dev. 67: 19–25, 2004. © 2004 Wiley‐Liss, Inc.