Prevention of lethal hepatic injury in Long-Evans Cinnamon (LEC) rats by D-galactosamine hydrochloride
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- Otsuka Toshihiro
- Department of Digestive and Pediatric Surgery, The University of Tokushima Graduate School
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- Izumi Keisuke
- Department of Molecular and Environmental Pathology, The University of Tokushima Graduate School
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- Tokunaga Itsuo
- Department of Legal Medicine, The University of Tokushima Graduate School
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- Gotohda Takako
- Department of Legal Medicine, The University of Tokushima Graduate School
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- Ipposhi Kaneshige
- Department of Clinical Pharmacology, Institute of Health Biosciences, The University of Tokushima Graduate School
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- Takiguchi Yoshiharu
- Department of Clinical Pharmacology, Institute of Health Biosciences, The University of Tokushima Graduate School
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- Kaneda Shinya
- Department of Molecular and Environmental Pathology, The University of Tokushima Graduate School
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- Satake Nobuo
- Department of Molecular and Environmental Pathology, The University of Tokushima Graduate School
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- Ohnishi Takamasa
- Department of Molecular and Environmental Pathology, The University of Tokushima Graduate School
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- Tashiro Seiki
- Department of Digestive and Pediatric Surgery, The University of Tokushima Graduate School
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- Shimada Mitsuo
- Department of Digestive and Pediatric Surgery, The University of Tokushima Graduate School
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抄録
Repeated injections of D-galactosamine hydrochloride (GalN) increase the survival rate of Long-Evans Cinnamon (LEC) rats, an animal model of Wilson’s disease. The aim of the present study was to investigate the mechanism of GalN for prevention of spontaneous lethal hepatic injury in LEC rats. Male LEC rats were given a single subcutaneous injection of 300 mg/kg of GalN or vehicle (0.9% NaCl) at 14 weeks, and killed at 28 weeks of age. Next, 6-week-old male LEC rats were given weekly subcutaneous injections of 300 mg/kg of GalN or vehicle for 3 or 12 weeks, and their hepatic 8-hydroxydeoxy-2’-guanosine (8-OHdG), glutathione peroxidase (GPX), and catalase activities were measured. None of GalN-treated rats died of hepatic injury (0/12), whereas the mortality rate of control rats given 0.9% NaCl was 17% (2/12). GalN administration for 12 weeks decreased the hepatic 8-OHdG, and GalN administration for either 3 or 12 weeks increased the glutathione peroxidase activity. GalN administration increased the serum level of alanine aminotransferase, and accelerated megalocytic degeneration of the hepatocytes. GalN treatment is effective in preventing lethal hepatitis in LEC rats and decrease of oxidative DNA damage by GalN plays an important role in increase of the survival rate. 53: 81-86, February, 2006
収録刊行物
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- The Journal of Medical Investigation
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The Journal of Medical Investigation 53 (1-2), 81-86, 2006
国立大学法人 徳島大学医学部
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詳細情報 詳細情報について
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- CRID
- 1390282679220414848
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- NII論文ID
- 110004748501
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- NII書誌ID
- AA11166929
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- ISSN
- 13496867
- 13431420
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- IRDB
- Crossref
- CiNii Articles
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- 抄録ライセンスフラグ
- 使用不可