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Prince Henrys Institute of Medical Research (L.O., K.M.R., M.E.J., E.R.S.) and Department of Biochemistry (K.M.R.), Monash University, Clayton, 3168, Victoria, Australia
Although it has been known for many years that estrogen administration
has deleterious effects on male fertility, data from transgenic mice
deficient in estrogen receptors or aromatase point to an essential
physiological role for estrogen in male fertility. This review
summarizes the current knowledge on the localization of estrogen
receptors and aromatase in the testis in an effort to understand the
likely sites of estrogen action. The review also discusses the many
studies that have used models employing the administration of
estrogenic substances to show that male fertility is responsive to
estrogen, thus providing a mechanism by which inappropriate exposure to
estrogenic substances may cause adverse effects on spermatogenesis and
male fertility. The reproductive phenotypes of mice deficient in
estrogen receptors
and/or ß and aromatase are also compared to
evaluate the physiological role of estrogen in male fertility. The
review focuses on the effects of estrogen administration or
deprivation, primarily in rodents, on the hypothalamo-pituitary-testis
axis, testicular function (including Leydig cell, Sertoli cell, and
germ cell development and function), and in the development and
function of the efferent ductules and epididymis. The requirement for
estrogen in normal male sexual behavior is also reviewed, along with
the somewhat limited data on the fertility of men who lack either the
capacity to produce or respond to estrogen. This review highlights the
ability of exogenous estrogen exposure to perturb spermatogenesis and
male fertility, as well as the emerging physiological
role of estrogens in male fertility, suggesting that, in this local
context, estrogenic substances should also be considered "male
hormones."
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X. Li, L. Strauss, S. Makela, T. Streng, I. Huhtaniemi, R. Santti, and M. Poutanen Multiple Structural and Functional Abnormalities in the P450 Aromatase Expressing Transgenic Male Mice Are Ameliorated by a P450 Aromatase Inhibitor Am. J. Pathol., March 1, 2004; 164(3): 1039 - 1048. [Abstract] [Full Text] [PDF] |
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O. M. Tirado, D. M. Selva, N. Toran, C. A. Suarez-Quian, M. Jansen, D. P. McDonnell, J. Reventos, and F. Munell Increased Expression of Estrogen Receptor {beta} in Pachytene Spermatocytes After Short-Term Methoxyacetic Acid Administration J Androl, January 1, 2004; 25(1): 84 - 94. [Abstract] [Full Text] [PDF] |
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S. Bourguiba, S. Chater, C. Delalande, M. Benahmed, and S. Carreau Regulation of Aromatase Gene Expression in Purified Germ Cells of Adult Male Rats: Effects of Transforming Growth Factor {beta}, Tumor Necrosis Factor {alpha}, and Cyclic Adenosine 3',5'-Monosphosphate Biol Reprod, August 1, 2003; 69(2): 592 - 601. [Abstract] [Full Text] [PDF] |
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J. Lassurguere, G. Livera, R. Habert, and B. Jegou Time- and Dose-Related Effects of Estradiol and Diethylstilbestrol on the Morphology and Function of the Fetal Rat Testis in Culture Toxicol. Sci., May 1, 2003; 73(1): 160 - 169. [Abstract] [Full Text] [PDF] |
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S. Ramaswamy, G. R. Marshall, C. R. Pohl, R. L. Friedman, and T. M. Plant Inhibitory and Stimulatory Regulation of Testicular Inhibin B Secretion by Luteinizing Hormone and Follicle-Stimulating Hormone, Respectively, in the Rhesus Monkey (Macaca mulatta) Endocrinology, April 1, 2003; 144(4): 1175 - 1185. [Abstract] [Full Text] [PDF] |
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R. Thuillier, Y. Wang, and M. Culty Prenatal Exposure to Estrogenic Compounds Alters the Expression Pattern of Platelet-Derived Growth Factor Receptors {alpha} and {beta} in Neonatal Rat Testis: Identification of Gonocytes as Targets of Estrogen Exposure Biol Reprod, March 1, 2003; 68(3): 867 - 880. [Abstract] [Full Text] [PDF] |
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K. Golovine, M. Schwerin, and J. Vanselow Three Different Promoters Control Expression of the Aromatase Cytochrome P450 Gene (Cyp19) in Mouse Gonads and Brain Biol Reprod, March 1, 2003; 68(3): 978 - 984. [Abstract] [Full Text] [PDF] |
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R. Nair and C. Shaha Diethylstilbestrol Induces Rat Spermatogenic Cell Apoptosis in Vivo through Increased Expression of Spermatogenic Cell Fas/FasL System J. Biol. Chem., February 14, 2003; 278(8): 6470 - 6481. [Abstract] [Full Text] [PDF] |
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