Apoptosis and Mitochondrial Damage in INS-1 Cells Treated with Alloxan.
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- SAKURAI Koichi
- Department of Biochemistry, Hokkaido College of Pharmacy
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- KATOH Mika
- Department of Biochemistry, Hokkaido College of Pharmacy
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- SOMENO Kimio
- Department of Biochemistry, Hokkaido College of Pharmacy
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- FUJIMOTO Yukio
- Department of Biochemistry, Hokkaido College of Pharmacy
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To evaluate the participation of mitochondrial damage, oxygen radicals and cell death in diabetes mellitus, we designed a way to investigate INS-1 cells, rat pancreatic β-cell line, to die by treatment with alloxan which generate reactive oxygen species (ROS). Incubation of INS-1 cells with alloxan for 24 h resulted in a decrease in viability of cells as well as inhibition of glucose-stimulated insulin release; this could be prevented by antioxidants, vitamin E and butylated hydroxyanisol (BHA). The formation of a DNA ladder and the distribution of phosphatidylserine at the external surface of plasma membrane were observed as indicators of apoptosis in the cells treated with alloxan at concentrations below 0.5 mM. The formation of DNA ladder was prevented by vitamin E, BHA and catalase, suggesting that the ROS is involved in the process of apoptosis in INS-1 cells treated with alloxan. Lower levels of intracellular ATP, collapse of mitochondrial membrane potential and release of cytochrome c from mitochondria were also observed in INS-1 cells treated with alloxan, suggesting that alloxan caused the damage of mitochondria in cells and was related to the process of apoptosis. In contrast, rat liver RLC-18 cells treated with alloxan were not observed in the decrease of viability. It follows from the present study that mitochondrial damages by ROS generated from alloxan is linked to apoptosis in INS-1 cells.
収録刊行物
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- Biological & Pharmaceutical Bulletin
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Biological & Pharmaceutical Bulletin 24 (8), 876-882, 2001
公益社団法人 日本薬学会
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詳細情報 詳細情報について
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- CRID
- 1390001204625181312
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- NII論文ID
- 110003638580
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- NII書誌ID
- AA10885497
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- COI
- 1:CAS:528:DC%2BD3MXlvVCms7c%3D
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- ISSN
- 13475215
- 09186158
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- NDL書誌ID
- 5852093
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- PubMed
- 11510477
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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
- NDL
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- PubMed
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- 使用不可