Project/Area Number |
12670910
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Radiation science
|
Research Institution | Kanazawa Medical University |
Principal Investigator |
MATOBA Munetaka Kanazawa. med. univ., medical course, lecturer, 医学部, 講師 (90288308)
|
Co-Investigator(Kenkyū-buntansha) |
YOKOTA Hajime Kanazawa. med. univ., medical course, lecturer, 医学部, 講師 (30182695)
|
Project Period (FY) |
2000 – 2001
|
Project Status |
Completed (Fiscal Year 2001)
|
Budget Amount *help |
¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2001: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 2000: ¥600,000 (Direct Cost: ¥600,000)
|
Keywords | degradable starch microsphere / animal study / ischemia / reperfusion / superoxide dismutase / DSM / 虚血再灌流障害 / VX2 / 実験腫瘍 / SOD / 活性酸素 |
Research Abstract |
In this study, rabbits with VX2 carcinoma received regional infusion of degradable starch microsphere(DSM) by transcatheter angiography, and it was confirmed that DSM occluded tumor vessels. Blood flow in the tumors decreased rapidly immediately after the DSM treatment and returned to the original level. We demonstrated that the antitumor effect was obtained by the infusion of DSM to the arteries by which the tumor tissues were fed. In the groups given the DSM for 30mg/kg by both single infusion and daily for 3 days, the tumor growth ratio was significantly different from the control group, tumor growth was significantly inhibited. The tumor growth ratio in the group given the DSM for 10mg/kg by daily for 3 days was inhibited to compare with the control group. In this study, the time course changes of the activity of superoxide dismutase(SOD) in the tumoral tissue were measured after injection of the DSM. The value of the activity of SOD was significantly decreased after re-perfusion of tumor tissue blood flow. In the muscles around the tumor, the same time course changes of the activity of SOD were observed. Pathologically, occlusion of the tumor vessels by thrombus was not observed. It was thought that the antitumor effect of the transient embolic agent DSM was secondary to the phenomenon of ischemic-reperfusion injury.
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