2000 Fiscal Year Final Research Report Summary
Toxic mechanisms of endocrine disrupting chemicals for reproductiue function.
| Project/Area Number |
11839024
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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 Institution | Keio University |
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Principal Investigator |
SUEOKA Kou Keio Univ., School of Medicine, Associate Professor, 医学部, 助教授 (90162833)
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| Co-Investigator(Kenkyū-buntansha) |
MATSUDA Noriko Keio Univ., School of Medicine, Instructor, 医学部, 助手 (80286541)
OHMAE Kazuyuki Keio Univ., School of Medicine, Professor, 医学部, 教授 (60118924)
YOSHIMURA Yasunori Keio Univ., School of Medicine, Professor, 医学部, 教授 (10129736)
TANIGAKI Reiko Keio Univ., School of Medicine, Instructor, 医学部, 助手 (00265852)
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| Project Period (FY) |
1999 – 2000
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| Keywords | c-kit / spermatogonia / W / + / W / W^v / W^v / + / maturation arrest / RT-PCR / immunohistochemistry |
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| Research Abstract |
The protooncogene of Tyrosin Kinase receptor c-kit was focused in the role of spermatogenic differentiation in testis. The implication of c-kit was examined on the aspect of gene expression and c-kit production at testicular germ cell by RT-PCR and immunohistochemistry. Hetero and homo mutant mice with two types of c-kit mutations were used for the experiments, which were W with 78 amino acids deletion and W^v with a point mutation at 790 amino acid sequence from N-terminal. Hetero mutant of W/+ and W^v/+, homo mutant of W/W^v were compared to wild type (+/+). Although c-kit m-RNA were expressed strongly at both hetero mutant and wild type, W/W^v testis expressed mutated gene. Anti-c-kit monoclonal antibody CD117 was used for immunohistochemical study. Whereas c-kit were expressed in Leidig cell of hetero and homo mutants, it was detected in spermatogonia of wild type and hetro mutants. In the protocol of present studies, testicular disfunction following exposure of toxic chemicals are determining at the mechanisms prouoked by c-kit and its gene experssion. These results suggested that c-kit had strongly implicated to the spermatogenesis especially at the differentiation of spermatogonia. This pathological status occured by the exposure of endocrine disrupting chemicals may affect the mechanisms of maturation arrest in male reproductive function.
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