Spermatogenic Germ Cell Apoptosis by Long-Term Sustained Delivery of b-Estradiol 3-benzoate in Rats
The correct mechanism of estrogen-induced spermatogenesis impairment is still not clear. In the present study, we investigated the role of long-term sustained delivery of β-estradiol 3-benzoate (EB) on spermatogenesis and possible mechanisms involved in which focused on the germ cell apoptosis. Tenw...
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Published in | Laboratory animal research pp. 111 - 117 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | Korean |
Published |
한국실험동물학회
01.03.2008
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Subjects | |
Online Access | Get full text |
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Summary: | The correct mechanism of estrogen-induced spermatogenesis impairment is still not clear. In the present
study, we investigated the role of long-term sustained delivery of β-estradiol 3-benzoate (EB) on
spermatogenesis and possible mechanisms involved in which focused on the germ cell apoptosis. Tenweek
old Sprague-Dawley rats were implanted subcutaneously with fused pellet containing of 0.5 mg EB
and were sacrificed at 12 hr, 24 hr, 48 hr, 72 hr, 1 week, 2 weeks, 4 weeks and 6 weeks. Body, testis, and
epididymis weights were significantly decreased from 2 weeks. Degenerating germ cells were first found
from 48 hr and progressively increased with time-dependent manner. At 2 weeks, germ cell depletion and
degeneration of spermatocytes were observed in the seminiferous tubules. At 4 and 6 weeks, massive
degenerating changes of the seminiferous tubules characteristics of epithelial structural disorganization
and multinucleated giant cells formation and decrease of interstitial cell number were noted. Apoptosis of
germ cells was identified in pachytene spermatocytes in stages VII-VIII from 48 hr. Mean number of
apoptotic germ cells were progressively increased and peaked at 2 weeks and then decreased but higher
than normal level. ERα expression was not changed but Fas and Fas lignad (FasL) protein levels were
increased in EB-treated rat. In conclusion, sustained increase level of estrogen was impaired
spermatogenesis with an increase of germ cell apoptosis mediated through modulation of Fas/FasL system
partially in which ERα may not play a significant role. KCI Citation Count: 1 |
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Bibliography: | G704-001509.2008.24.1.005 |
ISSN: | 1738-6055 2233-7660 |