Inhibitory action of oxidized lipoproteins on the activity of plasma lecithin-cholesterol acyltransferase and the effects of the atherosclerosis lesions.
| Project/Area Number |
09660128
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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 |
食品科学・栄養科学
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| Research Institution | Tohoku University |
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Principal Investigator |
FURUKAWA Yuji Tohoku Univ., Applied Biological Chemistry, Professor, 農学部, 教授 (60005626)
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| Co-Investigator(Kenkyū-buntansha) |
ITO Michiko Tohoku Univ., Applied Biological Chemistry, Research assistant, 農学部, 教務職員 (60250734)
KOMAI Michio Tohoku Univ., Applied Biological Chemistry, Associate professor, 農学部, 助教授 (80143022)
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| Project Period (FY) |
1997 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 1998: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1997: ¥2,400,000 (Direct Cost: ¥2,400,000)
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| Keywords | LCAT / oxidized LDL / oxidized sterol / anti-atherosclerolemic action / vitamin C / lipoproteins |
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| Research Abstract |
This study was designed to clarify the effects of free radical generation on the activity of lecithin-cholesterol acylyransferase(LCAT). A free radical initiator. 2,2'-azobis -amidino propane dihydrochloride(AAPH), inhibited the activity of plasma LCAT as a function of the incubation time after its addition. When the small amount of oxidized LDL or HDL were added to plasma, LCAT activity was dose dependently inhibited. To identify the effects of HDL oxidation on LCAT activity, a purified enzyme and cofactor in a vesicle solution(an artificial substrate) were used.
1) LCAT activity was inhibited by the oxidation of substrate vesicles, this inhivition being related to the degree of oxidation.
2) This inhibition was observed even if apolipoprotein A-I was not oxidized.
3) Oxidized phosphatidylcholine, but not oxidized cholesterol, in the vesicles affected LCAT activity.
4) The addition of 0-40% of oxidized vesicles to normal substrate vesicles resulted in the activity of LCAT being inhibited in a dose-dependent manner.
These result suggest that the esterification of cholesterol by LCAT may be affected by the oxidation of substrate phosphstidylcholine via free radical generation in the plasma.
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Report
(3 results)
Research Products
(4 results)
