STRESS AND TESTICULAR GERM CELL APOPTOSIS

Chronic immobilization stress provokes an increase in serum corticosterone, which causes the decline in testosterone concentration. The stress and glucocorticoid administration induce germ cell apoptosis in rat testes. The cell type that has been shown to undergo apoptosis is spermatogonia. Since a...

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Bibliographic Details
Published in:Archives of andrology 2001, Vol.47 (3), p.211-216
Main Authors: Sasagawa, I., Yazawa, H., Suzuki, Y., Nakada, T.
Format: Article
Language:English
Subjects:
Animals
Apoptosis
Apoptosis - physiology
Biological and medical sciences
Cricetinae
Fundamental and applied biological sciences. Psychology
Germ Cell
Glucocorticoid
Glucocorticoids - physiology
Immobilization - physiology
In Situ Nick-End Labeling
Male
Mammalian male genital system
Morphology. Physiology
Rats
Spermatogonia - physiology
Stress
Stress, Psychological - physiopathology
Testis
Testis - cytology
Testis - physiology
Vertebrates: reproduction
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Summary:Chronic immobilization stress provokes an increase in serum corticosterone, which causes the decline in testosterone concentration. The stress and glucocorticoid administration induce germ cell apoptosis in rat testes. The cell type that has been shown to undergo apoptosis is spermatogonia. Since a potent glucocorticoid receptor agonist completely suppressed glucocorticoid induced germ cell apoptosis, the regulation of transcription of gene mediated by the glucocorticoid receptor may enhance apoptosis of testicular germ cells. The apoptosis of testicular germ cells would involve certain specific gene activities and proteins, including Bc1-2 family, p53, and Fas. Molecular investigations may help to determine whether the different pathways possess mechanisms of germ cell apoptosis induced by somatic stress and glucocorticoids.
ISSN:0955-3002
0148-5016
1362-3095
1521-0375
DOI:10.1080/014850101753145924