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发生在我国与俄罗斯低硒地带的克山病(KSD)与大骨节病(KBD)的共同发病特点是细胞膜系统的氧化损伤及组织的早期老化。二者虽均属儿童多发,均处在组织低硒、谷胱甘肽过氧化物酶活性低、脂过氧化物增加的抗氧化能力降低、膜脂氧化损伤、磷脂减少的状态,但所侵害的组织器官不同,KBD主要侵害骨软骨以磷脂酰胆碱减少为主,KSD则侵害心肌,以心磷脂减少为主,细胞色素氧化酶活性降低。代表细胞膜老化指数的胆固醇/磷脂、鞘磷脂/胆碱磷脂、饱和脂酸/不饱和脂酸的分子比均增高,老化的棘细胞增加膜脆化,同时KSD的血脂、胆固醇(ch)、(LDL+VLDL)—Ch及动脉硬化指数增加。KBD软骨粘多糖的硫酸化程度降低及硫酸软骨素/胶原比下降等结缔组织老化改变。本研究再一次证明有关老化机制的自由基损伤学说,同时通过缺硒病组织早期老化机制的研究,探讨了推迟老化进程延长寿限的可能途径。
The common incidence of KSD and KDD in China and the Russian low selenium zone is characterized by oxidative damage of the cell membrane system and early tissue aging. Although both children are multiple, are in the organization of low selenium, glutathione peroxidase activity is low, increased lipid peroxidation decreased antioxidant capacity, lipid peroxidation, phospholipid lipid reduction, but the violation Different tissues and organs, KBD mainly infiltration of osteochondral to reduce the main phosphatidylcholine, KSD is harmful to the myocardium, mainly to reduce the cardiolipin, cytochrome oxidase activity decreased. The molecular ratios of cholesterol / phospholipid, sphingomyelin / choline phospholipid and saturated fatty acid / unsaturated fatty acid, which represent the index of cell membrane aging, were all increased. Aging cells increased membrane embolism, meanwhile, KSD’s blood lipids, cholesterol, LDL + VLDL) -Ch and arteriosclerosis index increased. KBD cartilage mucopolysaccharides decreased the degree of sulfation and chondroitin sulfate / collagen ratio decreased connective tissue aging changes. This study once again proves that the mechanism of free radical damage related to aging theory, at the same time through the early senescence mechanism of selenium deficiency disease mechanism to explore the possible ways to delay the aging process to extend the life limit.