Sulyok S, Bar-Pollák Z, Fehér E, Kemenes I, Kántor I, Fehér J
Acta Physiol Hung. 1984;64(3-4):437-42.
Lipid peroxidation has been induced by means of an atherogenic diet causing hypercholesterolaemia, hypertriglyceridaemia, increased LDL and decreased HDL serum fractions in addition to the fatty degeneration, vacuolization of the liver cells and accumulation of malondialdehyde in the liver. Increased release of acid phosphatase and N-beta-glucuronidase was also observed pointing to cholesterol-induced lysosomal membrane damage. In response to pretreatment with, and simultaneous administration of, 6,6'-methylene bis (2,2-dimethyl-4-methane sulphonic acid sodium salt-1,2-dihydroquinoline) the signs and symptoms of fatty liver degeneration, the tissue, plasma and platelet malondialdehyde concentrations and the LDL serum fraction significantly decreased and HDL serum fraction increased. Lisosomal membrane stability was restored, resulting in physiological acid phosphatase and N-beta-glucuronidase activities. The pathological and clinical aspects of lipid peroxidation in several diseases of the digestive organs and the suggested therapeutic uses of non-toxic radical scavengers have been outlined.
通过致动脉粥样化饮食诱导脂质过氧化，该饮食除了导致肝细胞脂肪变性、空泡化以及肝脏中丙二醛蓄积外，还会引起高胆固醇血症、高甘油三酯血症、血清低密度脂蛋白增加和高密度脂蛋白降低。还观察到酸性磷酸酶和N-β-葡萄糖醛酸酶的释放增加，这表明胆固醇诱导了溶酶体膜损伤。预先使用并同时给予6,6'-亚甲基双（2,2-二甲基-4-甲磺酸-1,2-二氢喹啉钠盐）后，脂肪肝变性的体征和症状、组织、血浆和血小板中的丙二醛浓度以及血清低密度脂蛋白部分显著降低，血清高密度脂蛋白部分增加。溶酶体膜稳定性得以恢复，从而使酸性磷酸酶和N-β-葡萄糖醛酸酶活性恢复正常。本文概述了消化器官几种疾病中脂质过氧化的病理和临床方面，以及无毒自由基清除剂的建议治疗用途。
