The role of cationized catalase and cationized glucose oxidase in mucosal oxidative damage induced in the rat jejunum.
1992; Elsevier BV; Volume: 267; Issue: 30 Linguagem: Inglês
10.1016/s0021-9258(19)36616-5
ISSN1083-351X
AutoresR. Kohen, Angel Kakunda, Abraham Rubinstein,
Tópico(s)Aldose Reductase and Taurine
ResumoThe successful prevention of hydrogen peroxide-induced damage to the rat jejunal mucosa by cationized catalase is described in this study.Biological damage was induced in a closed circulating intestinal loop of the rat by hydrogen peroxide and by hydroxyl radicals induced in situ via the metal-mediated Haber-Wiess reaction.The mucosal activity of lactate dehydrogenase and the amount of potassium ions were used to quantitatively characterize the tissue damage.Catalase was cationized by reacting it with N,N'-dimethyl-1,3-propanediamine to give a soluble product or with polyhistidine to give an insoluble product.The activity of the modified enzymes was assessed, and their ability to protect the rat jejunal mucosa against oxidative stress was studied.It was found that in all cases the cationized enzymes were superior to the native catalase in their shield capability.A significant protection against Fe(II)/H202 and ascorbic acid/copper ion-mediated damage was obtained when the cationized enzymes were used.In the presence of glucose, native glucose oxidase failed to cause damage in the rat jejunal mucosa; however, the cationized enzyme caused profound tissue injury.These findings indicate the potential therapeutic merit of cationized enzymes for the treatment of pathological processes in the intestine, whenever oxidative stress is involved.Reactive oxygen species such as hydrogen peroxide, superoxide radicals, hydroxyl radicals, and lipid peroxidation products are initiators of gastrointestinal epithelium injuries associated with inflammatory and ischemic bowel diseases, gastric ulceration, radiation enteritis, or colon cancer (1-4).Ischemic and post-ischemic processes in the intestinal vasculature, ingested food, catalase-negative bacteria, oxidases and substrate from sloughed cells, saliva, and cigarette smoke are possible sources for the hazardous oxygen metabolites (2).It was reported that the mucous lining of the gastrointestinal tract and of the tracheobronchial tissue possesses antioxidant properties (2, 5 ) .However, a continued exposure to efflux of
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