| Project/Area Number |
01571237
|
|---|
| Research Category |
Grant-in-Aid for General Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
医学一般
|
|---|
| Research Institution | University of the Ryukyus |
|---|
Principal Investigator |
MAEHIRA Fusako Univ. of Ryukyus, Faculty of Med., Assoc. Prof., 医学部, 助教授 (80045054)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
SHINJOH Sumie Univ. of Ryukyus, Faculty of Med., Assist. Prof., 医学部, 助手 (20154388)
|
|---|
| Project Period (FY) |
1989 – 1990
|
| Project Status |
Completed (Fiscal Year 1990)
|
| Budget Amount *help |
¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 1990: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1989: ¥1,000,000 (Direct Cost: ¥1,000,000)
|
|---|
| Keywords | Atherosclerosis / Cholesteryl esterases / Lipid peroxides / Oxidized-LDL / Rats / Human mononuclear leukocytes |
|---|
| Research Abstract |
A correlation between the degree of atherosclerotic change and the content of peroxidized fats in aorta had been demonstrated. In order to study a mechanism of interrelation between two variables, the rats were given a small quantity of linoleate hydroperoxide (LHPO) for 8 weeks. In the rats given LHPO, blood and hepatic lipid peroxides expressed as TBA values increased significantly whereas the activities of both acid and neutral cholesteryl esterases (AL and NL) in mononuclear leukocytes (MNL) and in aorta were decreased, together with increases of TBA values and cholesterol esters in aorta. Low density lipoprotein (LDL) isolated from th LHPO group exhibited high TBA values about 6 times the control LDL. It also showed characteristics typical to oxidized LDL ; a marked increase in negative electrophoretic mobility together with the degradation of the tertiary structure of apolipoprotein. The in vivo oxidized LDL of the LHPO group inhibited in vitro the AL and NL activities of aorta,
… More
MNL, and liver of the control group. The results in the animal experiment were confirmed by the cell culture study. The cigarette smoke-modified LDL (CS-LDL) and LDL isolated from type IIb hyperlipidemia (HC-LDL) which showed increased negative electrophoretic mobilities, and normal LDL (N-LDL), were added to the culture medium of normal MNL after each LDL was labeled with ^<125>I. Cellular bound and incorporation of LDL were great in order of CS-^<125>I-LDL, HC-^<125>I-LDL, and -^<125>I-LDL whereas cellular degradations of apoprotein of^<125>I-LDL were in the reverse order. Furthermore, both AL and NL activities in the same experiment were inhibited in the same way as the protein degradations of LDL by possibly lipid peroxides incorporated into the cell with LDL. The results suggest that the increased blood lipid peroxide alters LDL into oxidized form incorporated via macrophage receptors and it inhibits the cellular hydrolyzing enzymes of both protein and cholesterol esters of LDL, which may become one of factors in accelerating atherosclerotic changes of aorta. Less
|
