1997 Fiscal Year Final Research Report Summary
Cell Kinetics of Spermatogonia in the Testis with Hypospermatogenesis
| Project/Area Number |
07671742
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Urology
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| Research Institution | Sapporo Medical University School of Medicine |
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Principal Investigator |
HORITA Hiroki Sapporo Medical University School of Medicine Clinical Instructor, 医学部, 助手 (20260771)
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| Co-Investigator(Kenkyū-buntansha) |
TAKAGI Seiji Sapporo Medical University School of Medicine Clinical Instructor, 医学部, 助手
TACHIKI Hitoshi Sapporo Medical University School of Medicine Clinical Instructor, 医学部, 助手 (80236538)
MIKUMA Naoto Sapporo Medical University School of Medicine Clinical Instructor, 医学部, 助手 (30190614)
ITOH Naoki Sapporo Medical University School of Medicine Assistant Professor, 医学部, 講師 (60193504)
TSUKAMOTO Taiji Sapporo Medical University School of Medicine Professor, 医学部, 教授 (50112454)
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| Project Period (FY) |
1995 – 1997
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| Keywords | Spermatogenesis / Male Infertility / Spermatogonia / PCNA / Apoptosis / Apoptosis |
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| Research Abstract |
We have reported that some infertile males have a decreased number of spermatogonia but normal spermatogonial differentiation to spermatids. Proliferative dysfunction in the mitotic phase of accelerated germ-cell death might be a cause of the decreased number of spermatogonia. The aim of the current study is to analyze cell proliferation and apoptosis of spermatogonia in infertile males using immunohistochemical techniques. Fifty-nine patients, with either azoospermia or severe oligozoospermia, who underwent testicular biopsies in our clinic were included in this study. Cell proliferation was determined by the expression of proliferating cell nuclear antigen (PCNA) using a monoclonal antibody. Apoptosis was demonstrated by in situ analysis of DNA fragmentation (TUNEL method). Testicular histology was analyzed quantitatively in infertile men, who were divided into four subgroups by two parameters (the Sertoli cell ratio of spermatogonia and the ratio of the number of spermatids to the number of spermatogonia). The differences between each group and a control group consisting of histological findings and hormonal data (LH,FSH and testosterone). Of 59 infertile patients, 6 (10.2%) had a decreased number of spermatogonia without loss of spermatogenesis after proliferation of spermatogonia. Their serum FSH levels were not elevated (10.7(]SY.+-。[)9.8mIU/ml). The expression of PCNA was normal in all 6 patients but 2 of the 6 patients showed significantly higher levels of apoptosis than the control group. In this study, we demonstrated that some infertile males have a disorder of proliferation of proliferation of spermatogonial stem cells. The proliferative dysfunction in the mitotic phases, might induce the decreased number of spermatogonia in these patients. This decrease may not be associated with severe Sertoli cell dysfunction, as suggested by their normal FSH levels.
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