Document Detail


Protection from procarbazine-induced testicular damage by hormonal pretreatment does not involve arrest of spermatogonial proliferation.
MedLine Citation:
PMID:  9067277     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Hormone treatments that suppress sperm production enhance the recovery of spermatogenesis after gonadal exposure to various cytotoxic agents. It has generally been assumed that the mechanism of protection involved an arrest of spermatogonial kinetics. To test this hypothesis critically, we examined spermatogonial kinetics and numbers in rats in which the completion of spermatogenesis was suppressed with a 6-week testosterone plus 17beta-estradiol treatment that protected the testis from procarbazine-induced damage. Histological examination showed that the numbers of A-aligned, intermediate, and B spermatogonia and preleptotene spermatocytes and their mitoses were unaffected by testosterone plus 17beta-estradiol treatment. Flow cytometric analysis of bromodeoxyuridine-labeled cells showed that the percentage of diploid cells undergoing DNA synthesis, the progression of B spermatogonia and preleptotene spermatocytes through S-phase, the division of intermediate and B spermatogonia, the entry of intermediate spermatogonia into their next S-phase as type B cells, and the progression of cells through meiotic prophase were either unchanged or very slightly increased. Thus, changes in spermatogonial numbers or suppression of their proliferation cannot account for protection of spermatogenesis from exposure to cytotoxic agents.
Authors:
M L Meistrich; G Wilson; Y Zhang; B Kurdoglu; N H Terry
Related Documents :
20525087 - Postnatal testis development, sertoli cell proliferation and number of different sperma...
9067277 - Protection from procarbazine-induced testicular damage by hormonal pretreatment does no...
17884947 - Cellular defense mechanisms against benzo[a]pyrene in testicular leydig cells: implicat...
9582517 - Expression of oestrogen receptor beta (er beta) occurs in multiple cell types, includin...
7593267 - Growth and maturation of primary-cultured adipocytes from lean and ob/ob mice.
1064607 - Isoproterenol-induced changes in cell cycle kinetics of parotid gland acinar cells in 8...
Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Cancer research     Volume:  57     ISSN:  0008-5472     ISO Abbreviation:  Cancer Res.     Publication Date:  1997 Mar 
Date Detail:
Created Date:  1997-04-09     Completed Date:  1997-04-09     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  2984705R     Medline TA:  Cancer Res     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  1091-7     Citation Subset:  IM    
Affiliation:
Department of Experimental Radiation Oncology, The University of Texas M. D. Anderson Cancer Center, Houston 77030, USA.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Animals
Cell Division / drug effects
DNA Replication / drug effects
Drug Administration Schedule
Drug Implants
Estradiol / administration & dosage,  therapeutic use*
Growth Inhibitors / toxicity*
Infertility, Male / chemically induced*,  prevention & control
Male
Procarbazine / toxicity*
Rats
Spermatogenesis / drug effects*
Spermatogonia / drug effects*,  pathology
Testosterone / administration & dosage,  therapeutic use*
Grant Support
ID/Acronym/Agency:
CA-16672/CA/NCI NIH HHS; CA-17364/CA/NCI NIH HHS; ES-08075/ES/NIEHS NIH HHS
Chemical
Reg. No./Substance:
0/Drug Implants; 0/Growth Inhibitors; 50-28-2/Estradiol; 58-22-0/Testosterone; 671-16-9/Procarbazine

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Androgens stimulate fatty acid synthase in the human prostate cancer cell line LNCaP.
Next Document:  Methylenetetrahydrofolate reductase polymorphism, dietary interactions, and risk of colorectal cance...