인문학
사회과학
자연과학
공학
의약학
농수해양학
예술체육학
복합학
DBpia AI
AI 에이전트
AI 아이디어
AI 리더
AI 뷰어
Citeasy
크롬 서지관리 다운로드
개인구독
소속 기관이 없으신 경우, 개인 정기구독을 하시면 저렴하게
논문을 무제한 열람 이용할 수 있어요.
지원사업
학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
커뮤니티
연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
피인용 0
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.
본문·목차
인공지능 문자 인식 모델을 통해 추출된 텍스트로, 일부 오타나 오류가 포함될 수 있으나 지속적으로 개선 중입니다.
오류를 발견하셨다면 해당 부분을 드래그한 후 ' 를 통해 신고해주세요.
오류를 발견하셨다면 해당 부분을 드래그한 후 ' 를 통해 신고해주세요.
최근 본 자료 전체보기
UCI(KEPA) : I410-ECN-0101-2009-510-014753635
