| Project/Area Number |
62480207
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Neurology
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| Research Institution | Kyushu University |
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Principal Investigator |
GOTO Ikuo Kyushu University, Faculty of Medicine, Professor, 医学部, 教授 (20038631)
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| Co-Investigator(Kenkyū-buntansha) |
KOBAYASHI Takuro Kyushu University, Faculty of Medicine, Lecturer, 医学部, 講師 (40158902)
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| Project Period (FY) |
1987 – 1988
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| Project Status |
Completed (Fiscal Year 1988)
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| Budget Amount *help |
¥5,500,000 (Direct Cost: ¥5,500,000)
Fiscal Year 1988: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1987: ¥5,000,000 (Direct Cost: ¥5,000,000)
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| Keywords | Aging / toxic substance / psychosine / sphingosine / リゾスルファチド / 老化 / 毒性物質 / psychosine / 高速液体クロマトグラフィー / sphingosine |
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| Research Abstract |
Endogeneous toxic substance may cause the aging of the nervous tissue. It is well known that lysosphingolipids, deacylated forms of sphingolipids which are abundant in the nervous tissur, are highly toxic. We have developed assay methods of lysosphingolipids, and investi- gated metabolisms and biological functions of the lipids these two years. The principle of the assay method is to couple fluorescent probe with the primary amine in lysosphingolipids and to detect fluorescent lysosphingolipids using high-performance liquid chromatography. Using this method, we demonstrated an occurrence of free sphingoid base and galactosylsphingo-sine (psychosine) in normal mouse and human tissues. Concentrations of psychosine increased with age, while those of free sphingoid bases did not change during developmental periods. Further studies on the concentration of lysosphingolipids in nervous tissues of aged human or animal subjects are currently under way.
As to the toxicity of lysosphingolipids, we found a close relationship of psychosine accumulation and the demyelination, occurring in globoid cell leukodystrouphy. In the twitcher mouse, an animal model of human globoid cell leukodystrophy, fatty acylation of myelin proteo-lipid protein was desturbed, probably because of an accumulation of spychosine in the myelin. We reported that lysosulfatide inhibited cytochrome C oxidase activity.
Further studies concerning physiological functions and metabolisms of lysosphingolipids in tissues from normal and aged subjects will be necessary.
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