Tesco G, Latorraca S, Piersanti P, Sorbi S, Piacentini S, Amaducci L
Department of Neurology, University of Florence, Italy.
Ann N Y Acad Sci. 1992 Dec 26;673:149-53. doi: 10.1111/j.1749-6632.1992.tb27446.x.
Oxygen radical production is postulated to be a major cause of cell damage in aging. We have studied the response to toxic oxygen metabolites of fibroblast cell lines derived from skin biopsies of patients with familial and sporadic Alzheimer's disease compared with those derived from normal controls. Fibroblasts were damaged by the generation of oxygen metabolites during the enzymatic oxidation of acetaldehyde by 50 mU of xanthine-oxidase. To quantify cell damage we measured lactate dehydrogenase activity in the culture medium and cell viability in fibroblast cultures from four normal subjects, five FAD, and four AD patients after 2 hours of Xo incubation. We found a significant increase of LDH activity in FAD vs. controls and also in AD vs. controls, suggesting that AD cells are more susceptible to oxygen radical damage than are normal controls.
氧自由基的产生被认为是衰老过程中细胞损伤的主要原因。我们研究了来自家族性和散发性阿尔茨海默病患者皮肤活检的成纤维细胞系对有毒氧代谢产物的反应，并与来自正常对照的细胞系进行了比较。在50 mU黄嘌呤氧化酶对乙醛进行酶促氧化过程中，氧代谢产物的产生会损伤成纤维细胞。为了量化细胞损伤，我们在黄嘌呤氧化酶孵育2小时后，测量了四名正常受试者、五名家族性阿尔茨海默病患者和四名散发性阿尔茨海默病患者的成纤维细胞培养物中培养基中的乳酸脱氢酶活性和细胞活力。我们发现，与对照组相比，家族性阿尔茨海默病患者和散发性阿尔茨海默病患者的乳酸脱氢酶活性均显著增加，这表明阿尔茨海默病细胞比正常对照细胞更容易受到氧自由基损伤。
