Hydroxyl Radical is the Major Causative Factor in Stress-Induced Gastric Ulceration

摘要: The role of the metal-catalyzed production hydroxyl radicals (OH.) on gastric ulceration caused by restraint-cold stress in rat was studied. Stress causes a 50% increase thiobarbituric acid reactive species (TBARS) as measure lipid peroxidation, nearly 70% protein oxidation measured its carbonyl content and about 40% decrease glutathione fundic stomach, suggesting oxidative damage stress. also time-dependent mitochondrial superoxide dismutase activity peroxidase activity, both which correlate well with severity ulcer index. Specific OH. scavengers such benzoate or dimethylsulfoxide (DMSO) free radical trap alpha-phenyl N-tert-butyl nitrone (PBN) significantly inhibit this damage. Desferrioxamine (DFO), nontoxic transition metal ion chelator, protects mucosa against stress-ulceration dose dependently. Increased level TBARS inactivation are prevented DFO antioxidants vitamin E, critical A generating system constituted Cu2+, H2O2 ascorbate (reducing equivalent O2-) purified vitro, can be effectively DFO. stress-induced activation is completely blocked pretreatment alpha-amanitin indicating an increased synthesis enzyme transcription m-RNA. Quantitative measurement indicates that fivefold generation OH., correlates index progress results indicate consequence mucosa. This generated through Haber-Weiss reaction between O2- H2O2, latter being formed stimulation peroxidase.