Role of oxidative stress and antioxidant enzymes in Crohn's disease.

Autores de IIS La Fe

• Marisa Iborra Colomino

  Autor

• Inés Moret Tatay

  Autor

• Francisco Rausell Palamos

  Autor

• Guillermo Bastida Paz

  Autor

• Mariam Aguas Peris

  Autor

• Elena Cerrillo Bataller

  Autor

• 

  Pilar Nos Mateu

  Autor

• Belén Beltrán Niclós

  Autor

Grupos

• Enfermedad Inflamatoria Intestinal

Abstract

There is increasing interest in oxidative stress being a potential aetiological factor and/or a triggering factor in Crohn's disease, rather than a concomitant occurrence during the pathogenesis of the disease. Recent research has shown that the immune mononuclear cells of Crohn's disease patients are induced to produce hydrogen peroxide (H2O2). Similarly, the regulation of antioxidant enzymes during disease in these cells has been unravelled, showing that SOD (superoxide dismutase) activity and GPx (glutathione peroxidase) activity is increased during active disease and returns to normal in remission phases. However, catalase remains constantly inhibited which supports the idea that catalase is not a redox-sensitive enzyme, but a regulator of cellular processes. ROS (reactive oxygen species) can be produced under the stimulus of different cytokines such as TNFa (tumour necrosis factor a). It has been shown in different experimental models that they are also able to regulate apoptosis and other cellular processes. The status of oxidative stress elements in Crohn's disease and their possible implications in regulating cellular processes are reviewed in the present paper.