| Project/Area Number |
03454110
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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 |
Applied veterinary science
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| Research Institution | Hokkaido University |
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Principal Investigator |
MAEDE Yoshimitsu Hokkaido University, Faculty of Veterinary Medicine, Professor, 獣医学部, 教授 (40002084)
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| Co-Investigator(Kenkyū-buntansha) |
INABA Mutsumi Hokkaido University, Faculty of Veterinary Medicine, Lecturer, 獣医学部, 講師 (00183179)
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| Project Period (FY) |
1991 – 1992
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| Project Status |
Completed (Fiscal Year 1992)
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| Budget Amount *help |
¥5,900,000 (Direct Cost: ¥5,900,000)
Fiscal Year 1992: ¥1,600,000 (Direct Cost: ¥1,600,000)
Fiscal Year 1991: ¥4,300,000 (Direct Cost: ¥4,300,000)
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| Keywords | Babesia / Piroplasma / Anemia / Dogs / Erythrocytes / Macrophage / Erythrophagocytosis / Babesia gibsoni / 酸化障害 |
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| Research Abstract |
In order to establishethe effective therapy and prevention for piroplasmosis in domestic animals, we investigated the mechanism of anemia induced by Babesia gibsoni in dogs. The results were as follows. 1.Babesia gibsoni was successfully cultured in a settled layer of canine erythrocytes. 2. During the cultivation, the concentrations of methemoglobin and malondialdehyde, an end product of lipid peroxidation, in erythrocytes were significantly increased. 3. Glucose consumption and lactate production by infected erythrocytes, and 2,3-DPG concentration were also increased. 4. Erythrocyte deformability was decreased. 5. The erythrophagocytic activity of macrophages obtained from the peripheral blood of the infected dogs showed a marked increase in association with progressive parasitemia. 6. Administration of prednisolone to the infected dogs resuted in a transient recovery from anemia in these dogs. 7. The erythrophagocytic activity of macrophages was not suppressed by the administration of prednisolone in the infected dogs. These results indicate that erythrocytes infected with B.gibsoni were suffered from an oxidative damage by the multiplication of the parasites, and that the erythrophagocytic activity of macrophages against the damaged erythrocytes might be accelerated in infected dogs, resulting in anemia in these dogs.
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