論文

査読有り
2008年4月

Increased susceptibility to oxidant-mediated tissue injury and peritoneal fibrosis in acatalasemic mice

American Journal of Nephrology
  • Naomi Fukuoka
  • Hitoshi Sugiyama
  • Tatsuyuki Inoue
  • Yoko Kikumoto
  • Kei-ichi Takiue
  • Hiroshi Morinaga
  • Kazushi Nakao
  • Yohei Maeshima
  • Masato Asanuma
  • Da-Hong Wang
  • Keiki Ogino
  • Noriyoshi Masuoka
  • Hirofumi Makino
  • 全て表示

28
4
開始ページ
661
終了ページ
668
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1159/000121357
出版者・発行元
KARGER

Background: Peritoneal fibrosis is a major complication leading to the loss of peritoneal function in patients undergoing peritoneal dialysis. However, the effect of catalase depletion on peritoneal fibrosis has not yet been investigated. Methods: The impact of catalase deficiency on progressive peritoneal fibrosis has been studied in homozygous acatalasemic mutant mice or control wild-type mice by intraperitoneal injection of chlorhexidine gluconate (CG) every other day for 14 days. Results: The CG injections resulted in a thicker peritoneal membrane, reflecting peritoneal fibrosis with accumulation of interstitial type I collagen, peritoneal deposition of lipid peroxidation products (4-hydroxy-2-nonenal and 4-hydroxy-2-hexenal), and an elevated level of 8-hydroxy-2'-deoxyguanosine in peritoneal fluid in both mouse groups on day 14. The extent of these changes, however, was significantly higher in acatalasemic mice than in wild-type mice. The level of catalase activity remained low in the acatalasemic peritoneum without the compensatory upregulation of glutathione peroxidase, but with an insufficient upregulation of superoxide dismutase activity in CG-injected mice. Conclusions: Acatalasemia, therefore, exacerbates oxidant tissue injury and induces the peritoneum to develop irreversible fibrosis which is the most important complication of peritoneal dialysis. This study suggests that catalase plays a crucial role in the defense against oxidant-mediated peritoneal injury in a mouse peritoneal fibrosis model. Copyright (C) 2008 S. Karger AG, Basel.

リンク情報
DOI
https://doi.org/10.1159/000121357
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000255896200016&DestApp=WOS_CPL
ID情報
  • DOI : 10.1159/000121357
  • ISSN : 0250-8095
  • Web of Science ID : WOS:000255896200016

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