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Gestational and Lactational Exposure of Male Mice to Diethylstilbestrol Causes Long-Term Effects on the Testis, Sperm Fertilizing Ability In Vitro, and Testicular Gene Expression Mark R. Fielden, Robert G. Halgren, Cora J. Fong, Christophe Staub, Larry Johnson, Karen Chou, Tim R. Zacharewski Abstract The objective of the study was to determine the long-term effects of
gestational and lactational exposure to diethylstilbestrol (DES; 0,
0.1, 1, 10 µg/kg maternal body weight) on mouse testicular growth,
epididymal sperm count, in vitro fertilizing ability, and testicular
gene expression using cDNA microarrays and real-time PCR in mice on
postnatal day (PND) 21, 105 and 315. In the high dose group, there was
a persistent decrease in the number of Sertoli cells, and sperm count
was decreased on PND315 (p<0.05). Sperm motion was unaffected, however,
in vitro fertilizing ability of epididymal sperm was decreased in the
high dose group on both PND105 (p<0.001) and PND315 (p<0.05).
Early and latent alterations in the expression of genes involved in
estrogen signaling (ER Data Set Normalized expression values for control and DES-exposed animals for PND21, 105 and 315, including associated ratios (SD,N,SE), t-statistics, p-values and adjusted p-values, with gene names and Unigene cluster IDs. The data was post-processed using the GP3 script. Protocols The following link provides the various different microarray protocols.
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steroidogenesis (SF-1, Cyp17, Cyp11a, Star, SR-B1), lysosomal function
(LGP85, Psap), and regulation of testicular development (Tr2-11, Inhbc,
Hoxa10) were confirmed by real-time PCR. The results demonstrate that
early exposure to DES causes long-term adverse effects on testicular
development and sperm function, and these effects are associated with
changes in testicular gene expression, even long after the cessation
of DES exposure.