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자료유형
학술저널
저자정보
저널정보
한국실험동물학회 Laboratory Animal Research Laboratory Animal Research Vol.24 No.1
발행연도
수록면
111 - 117 (7page)

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초록· 키워드

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.
#Estrogen #apoptosis #spermatogenesis #Fas/FasL #estrogen receptor
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목차

  1. Materials and Methods
  2. Results
  3. Discussion
  4. Acknowledgment
  5. References

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