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dc.contributor.authorGu, Yi-Qunen_US
dc.contributor.authorBremner, William J.en_US
dc.contributor.authorBalourdos, Georgiaen_US
dc.contributor.authorMcLachlan, Robert I.en_US
dc.contributor.authorRobertson, David M.en_US
dc.contributor.authorWreford, Nigel G.en_US
dc.contributor.authorO'Donnell, Lizaen_US
dc.contributor.authorNarula, Anitaen_US
dc.date.accessioned2008-10-17T20:41:10Z
dc.date.available2008-10-17T20:41:10Z
dc.date.issued2001-04en_US
dc.identifier.citationJ Clin Endocrinol Metab. 2001 Apr;86(4):1814-22en_US
dc.identifier.urihttp://hdl.handle.net/1773/4337
dc.description.abstractHuman male hormonal contraceptive regimens do not consistently induce azoospermia, and the basis of this variable response is unclear. This study used nine adult macaque monkeys (Macaca fascicularis) given testosterone (T) implants for 20 weeks to study changes in germ cell populations in relation to sperm output. Germ cell numbers were determined using the optical disector stereological method. Four animals achieved consistent azoospermia (azoo group), whereas five animals did not (nonazoo group). T-induced gonadotropin suppression in all animals decreased A pale (Ap) spermatogonia to 45% of baseline within 2 weeks, leading to decreased B spermatogonia (32--38%) and later germ cells (20--30%) after 14 and 20 weeks. Though the reduction in later germ cell types could be primarily attributed to the loss of spermatogonia, the data suggested that some cells were lost during the spermatocyte and spermatid phase of development. B spermatogonial number was more markedly suppressed in azoospermic animals, compared with the nonazoo group, as was the conversion ratio between Ap and B spermatogonia. Abnormal retention of elongated spermatids (failed spermiation) was also prominent in some animals after long-term T administration. We conclude that: 1) the variable suppression of sperm output is attributed to the degree of inhibition of germ cell development from type B spermatogonia onwards, and this is related to the degree of FSH suppression; and 2) inhibition of Ap and B spermatogonial development and of spermiation are the major defects caused by long-term T administration to monkeys.en_US
dc.language.isoen_USen_US
dc.publisherThe Endocrine Societyen_US
dc.subjectmale contraceptionen_US
dc.subjecttestosteroneen_US
dc.subjectandrologyen_US
dc.subject5-alpha reductase inhibitorsen_US
dc.subjectgonadotropinsen_US
dc.subject.meshLuteinizing Hormone, blooden_US
dc.subject.meshGonadotropins, antagonists & inhibitorsen_US
dc.subject.meshMaleen_US
dc.subject.meshSertoli Cells, physiologyen_US
dc.subject.meshMacaca fascicularisen_US
dc.subject.meshTestosterone, pharmacokinetics, pharmacologyen_US
dc.subject.meshSperm Counten_US
dc.subject.meshSpermatogonia, classification, drug effects, physiologyen_US
dc.subject.meshResearch Support, Non-U.S. Gov'ten_US
dc.subject.meshFollicle Stimulating Hormone, blooden_US
dc.subject.meshGonadal Steroid Hormones, pharmacokinetics, pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshSpermatozoa, cytology, drug effects, physiologyen_US
dc.titleImpairment of Spermatogonial Development and Spermiation after Testosterone-Induced Gonadotropin Suppression in Adult Monkeys (Macaca fascicularis)en_US
dc.typeArticleen_US


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