1996 Fiscal Year Final Research Report Summary
The suppressive effect of a cytosolic Ca^<2+> chelator in superoxide-induced hepatocyte injury
| Project/Area Number |
07670594
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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 |
Gastroenterology
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| Research Institution | Okayama University |
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Principal Investigator |
UKIDA Minoru Okayama University, Medical Shool, Lecturer, 医学部・附属病院, 講師 (70151842)
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| Co-Investigator(Kenkyū-buntansha) |
MORIMOTO Youichi Okayama University, Medical Shool, Researcher, 医学部・附属病院, 医員
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| Project Period (FY) |
1995 – 1996
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| Keywords | Oxidative stress / Lipid peroxidation / Calcium-ion homeostasis / Hepatocellular injury / Liver perfusion / Cyclosporin A / Superoxide / Mitochondorial membrane potential |
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| Research Abstract |
In the study using primary cultured hepatocyrte, the cytosolic calcium ion chelator, 1,2-bis (O-aminophenoxy) ethane -N,N,N', N'-tetraacetic acid- acetoxymethylester (BAPTAAM) suppressed the hepatocellular injury by tert-butyl hydroperoxide (TBHP) at each extracellular calcium ion concentration of 0,1 and 3mM,indepent of the lipid peroxidation of the cell membrane and the mitochondrial membrane potential measured by Rhodamine 123. Therefore, the disturbance of cytosolic calcium homeostasis plays the major role in the hepatocellular injury by TBHP.
In the study using isolated liver perfusion, the the hepatocellular injury by TBHP was minimum in the physiological perfusate Ca^<2+> concentration of 1.25mM compared with those of 0mM and 2.50mM.Under the each perfusate Ca^<2+> concentrations, Cyclospolin A (CsA) suppressed significantly the hepatocyte cell death. About the mechanism of the suppressive effect of CsA,a conclusion could not be drawn yet, since the present experimental sample was very small.
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