Article Text

PDF

A novel antiulcerogenic stable radical prevents gastric mucosal lesions in rats.
  1. D Rachmilewitz,
  2. F Karmeli,
  3. E Okon,
  4. A Samuni
  1. Department of Medicine, Hadassah University Hospital, Mount Scopus, Jerusalem, Israel.

    Abstract

    The pathogenesis of gastric mucosal injury is still poorly understood. Recent reports implicate redox active metals and reactive oxygen species as mediators of gastric damage induced by ethanol or non-steroidal anti-inflammatory drugs. Attempts were made therefore to prevent gastric injury using chelators and the antioxidant enzymes catalase and superoxide dismutase. These attempts, at best, would only detoxify extracellular reactive species, such as those produced by activated circulating granulocytes and macrophages. This study utilises another strategy by pre-emption of both intra and extracellular reactive species using radical-radical annihilation reactions and by detoxifying redox active transition metals. Nitroxide, stable free radicals were shown to enter mucous cells, protect against the ethanol induced damage, and prevent gastric lesions induced by aspirin, indomethacin, 25% NaCl, or 0.6 N HCl. These findings confirm that gastric mucosal damage from the above agents is mediated by free radicals and, moreover, introduce a prototypical agent within a potential new class of gastric ulcer preventing drugs.

    Statistics from Altmetric.com

    Request permissions

    If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.