Mitochondrial disorders in NSAIDs-induced small bowel injury

• Watanabe Toshio

  Department of Gastroenterology, Osaka City University Graduate School of Medicine

• Tanigawa Tetsuya

  Department of Gastroenterology, Osaka City University Graduate School of Medicine

• Nadatani Yuji

  Department of Gastroenterology, Osaka City University Graduate School of Medicine

• Otani Koji

  Department of Gastroenterology, Osaka City University Graduate School of Medicine

• Machida Hirohisa

  Department of Gastroenterology, Osaka City University Graduate School of Medicine

• Okazaki Hirotoshi

  Department of Gastroenterology, Osaka City University Graduate School of Medicine

• Yamagami Hirokazu

  Department of Gastroenterology, Osaka City University Graduate School of Medicine

• Watanabe Kenji

  Department of Gastroenterology, Osaka City University Graduate School of Medicine

• Tominaga Kazunari

  Department of Gastroenterology, Osaka City University Graduate School of Medicine

• Fujiwara Yasuhiro

  Department of Gastroenterology, Osaka City University Graduate School of Medicine

• Arakawa Tetsuo

  Department of Gastroenterology, Osaka City University Graduate School of Medicine

抄録

Recent studies using small bowel endoscopy revealed that non-steroidal anti-inflammatory drugs including low-dose aspirin, can often induce small bowel injury. Non-steroidal anti-inflammatory drugs-induced small bowel mucosal injury involves various factors such as enterobacteria, cytokines, and bile. Experimental studies demonstrate that both mitochondrial disorders and inhibition of cyclooxygenases are required for development of non-steroidal anti-inflammatory drugs-induced small bowel injury. Mitochondrion is an organelle playing a central role in energy production in organisms. Many non-steroidal anti-inflammatory drugs directly cause mitochondrial disorders, which are attributable to uncoupling of oxidative phosphorylation induced by opening of the mega channel called mitochondrial permeability transition pore on the mitochondrial membrane by non-steroidal anti-inflammatory drugs. Bile acids and tumor necrosis factor-α also can open the permeability transition pore. The permeability transition pore opening induces the release of cytochrome c from mitochondrial matrix into the cytosol, which triggers a cascade of events that will lead to cell death. Therefore these mitochondrial disorders may cause disturbance of the mucosal barrier function and elevation of the small bowel permeability, and play particularly important roles in early processes of non-steroidal anti-inflammatory drugs-induced small bowel injury. Although no valid means of preventing or treating non-steroidal anti-inflammatory drugs-induced small bowel injury has been established, advances in mitochondrial studies may bring about innovation in the prevention and treatment of this kind of injury.<br>

収録刊行物

• Ｊｏｕｒｎａｌ　ｏｆ　Ｃｌｉｎｉｃａｌ　Ｂｉｏｃｈｅｍｉｓｔｒｙ　ａｎｄ　Ｎｕｔｒｉｔｉｏｎ

  Ｊｏｕｒｎａｌ　ｏｆ　Ｃｌｉｎｉｃａｌ　Ｂｉｏｃｈｅｍｉｓｔｒｙ　ａｎｄ　Ｎｕｔｒｉｔｉｏｎ 48 (2), 117-121, 2011

  一般社団法人　日本酸化ストレス学会

キーワード

• oxidative phosphorylation
• uncoupling
• mitochondrial permeability transition
• aspirin

詳細情報

• CRID: 1390282679647588352
• NII論文ID: 130004466628
• DOI: 10.3164/jcbn.10-73
• ISSN: 18805086
• ISSN: 09120009
• Web Site: https://search.jamas.or.jp/link/ui/2011323679
• 本文言語コード: en
• データソース種別:
  • JaLC
  • Crossref
  • CiNii Articles
• 抄録ライセンスフラグ: 使用不可