Jávor T, Past T, Nagy L, Mózsik G, Wittmann I
First Department of Medicine, Medical University, Pécs, Hungary.
Acta Physiol Hung. 1989;73(2-3):323-30.
Oxygen free radicals can be blamed for evoking gastric mucosal damage, because of the protective effect of some lipid soluble free radical scavengers (vitamin A related compounds, Vitamin E). Direct determination of free oxygen radicals related chemical entities in the gastric tissue during ulcerogenesis yielded controversial results. Aluminum antacid compound together with acid binding property exhibited cytoprotection too, elevating the tissue PGE2 level substantially. Magnesium containing antacid according to our model experiments on red blood cells damage by free radicals, is capable to bind free radicals as well as to counteract with the dangerous intracellular calcium accumulation. It has been concluded that aluminum-magnesium antacid has a cytoprotective effect via: 1. acid binding; 2. prostaglandin generation; 3. free radical scavenging; 4. calcium antagonist activity.
氧自由基可被认为是引起胃黏膜损伤的原因,因为一些脂溶性自由基清除剂(维生素A相关化合物、维生素E)具有保护作用。在溃疡形成过程中直接测定胃组织中与游离氧自由基相关的化学物质,结果存在争议。铝抗酸化合物除了具有酸结合特性外,还表现出细胞保护作用,能显著提高组织中前列腺素E2的水平。根据我们关于自由基对红细胞损伤的模型实验,含镁抗酸剂既能结合自由基,又能对抗危险的细胞内钙积累。得出的结论是,铝镁抗酸剂通过以下方式发挥细胞保护作用:1. 酸结合;2. 前列腺素生成;3. 自由基清除;4. 钙拮抗剂活性。