Document Detail

Gonadotropin-releasing hormone induction of apoptosis in the testes of goldfish (Carassius auratus).
MedLine Citation:
PMID:  15564332     Owner:  NLM     Status:  MEDLINE    
Apoptosis, or programmed cell death, can occur via death receptor or mitochondrial pathways. Normal spermatogenesis in mammals involves apoptosis mediated, in part, by the death receptor fas and its ligand. The regulation of programmed cell death in the gonads has been shown to be dependent on a number of locally produced factors, including GnRH. Whereas the role of GnRH in the control of apoptosis and follicular atresia has been documented in the mammalian ovary, GnRH regulation of testicular apoptosis remains obscure. A previous study in our laboratory demonstrated the involvement of GnRH on the induction of DNA fragmentation in mature, perispawning testis. In this study, we tested the hypothesis that GnRH plays a differential regulatory role during male gamete maturation by studying the effect of GnRH on the induction of apoptosis during goldfish spermatogenesis. Treatment with GnRH resulted in DNA fragmentation only during late stages of spermatogenesis as assessed by oligonucleotide detection and terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labeling assays. The GnRH-induced apoptosis in the goldfish testis was found to be mediated by increased levels of fas and fas ligand-like proteins as well as elevated activity of caspase-3 (an executioner caspase) and -8 (a death receptor-activated caspase). The results suggest the involvement of the death receptor pathway in GnRH-induced apoptosis, providing support for the hypothesis that GnRH plays an important role in the control of spermatogenesis in the goldfish testis.
Claudia V Andreu-Vieyra; Andre G Buret; Hamid R Habibi
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2004-11-24
Journal Detail:
Title:  Endocrinology     Volume:  146     ISSN:  0013-7227     ISO Abbreviation:  Endocrinology     Publication Date:  2005 Mar 
Date Detail:
Created Date:  2005-02-16     Completed Date:  2005-04-04     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0375040     Medline TA:  Endocrinology     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1588-96     Citation Subset:  AIM; IM    
Department of Biological Sciences, University of Calgary, Biosciences 282, 2500 University Drive NW, Calgary, Alberta, Canada T2N 1N4.
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MeSH Terms
Antigens, CD95 / metabolism
Blotting, Western
Caspase 3
Caspase 8
Caspases / metabolism
DNA / chemistry
DNA Fragmentation
Dose-Response Relationship, Drug
Enzyme Activation
Gonadotropin-Releasing Hormone / metabolism*
In Situ Nick-End Labeling
Ovary / metabolism
Receptors, LHRH / metabolism
Testis / metabolism*,  pathology*
Time Factors
Reg. No./Substance:
0/Antigens, CD95; 0/GNRHR2 protein, human; 0/Ligands; 0/Receptors, LHRH; 33515-09-2/Gonadotropin-Releasing Hormone; 9007-49-2/DNA; EC 3.4.22.-/CASP3 protein, human; EC 3.4.22.-/CASP8 protein, human; EC 3.4.22.-/Caspase 3; EC 3.4.22.-/Caspase 8; EC 3.4.22.-/Caspases

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

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