| Project/Area Number |
13671470
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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 |
Cerebral neurosurgery
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| Research Institution | Tokyo Medical University |
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Principal Investigator |
NISHIOKA Hiroshi Tokyo Medical University, Medicine, Assistant Professor, 医学部, 講師 (60218120)
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| Co-Investigator(Kenkyū-buntansha) |
SANO Tetsuro Tokyo Medical University, Medicine, Assistant, 医学部, 助手 (20322464)
HARAOKA Jo Tokyo Medical University, Medicine, Professor (chief), 医学部, 教授 (40090641)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 2002: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | Pituitary gland / Pituitary adenomas / Mitochondria / Aging / 放射線照射 |
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| Research Abstract |
We investigated changes of the mitochondria in the anterior pituitary ceils associated with aging and tumor formation. Following results were obtained: (1) Pituitary cells have a high potential to induce MnSOD, an atntioxidant metalloenzymes that exist in mitochondria, by oxidative stress. (2) Basal activities of SODs and mitochondrial enzymes do not decrease associated with aging. (3) Oncocytic change, that lead to a decreased endocrine activity, increase with advancing age in both normal and neoplastic pituitaries. (4) Oxidative stress can cause metabolic dysfunction of mitochondria, resembling those in oncocytic changes, and results in a decreased endocrine activity. (5) Oxidative stress can damage mitochondria! DNA. However, overall amount of mutantmitochondrial DNA is small and the presence of mutations in old people and in tumors might not always results in mitochondrial dysfunction.
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