血氧饱和度降低可促进红细胞氧化损伤  

Increased Oxidative Damages of Erythrocytes Caused by Declined Blood Oxygen Saturation

作　　者：赵勇[1] 兰珂[1] 王翔[1] 邓雪茹[1] 熊延连[1] 唐金龙[1] 

机构地区：[1]重庆大学生物工程学院,重庆400044

出　　处：《生物医学工程学杂志》2012年第2期323-327,共5页Journal of Biomedical Engineering

基　　金：国家自然科学基金资助项目(11072275);中央高校基本科研业务费资助项目(CDJXS 10231121)

摘　　要：研究氧化应激条件下,血氧饱和度(SO2)对红细胞氧化损伤的影响。体外将红细胞孵育至SO2分别为0.3、0.5、0.7、0.9及0.98等状态,加入终浓度为0.15mmol/L叔丁基过氧化氢(BHP)使其发生氧化应激反应。测量胞内还原性谷胱甘肽(GSH)含量反映细胞抗氧化力,以胞内高铁血红蛋白(MetHb)、膜质过氧化(TBARS)及膜上沉淀的变性珠蛋白链水平体现细胞氧化损伤程度。结果显示,BHP存在的条件下,GSH含量随SO2上升而增加;MetHb、TBARS及膜上珠蛋白链水平则随SO2的上升而下降。上述结果表明,氧化应激条件下,红细胞抗氧化力和氧化损伤与SO2密切相关,SO2的降低可促进红细胞氧化损伤。This paper was to explore the effect of blood oxygen saturation（SO2） on oxidative damages of erythrocytes under the condition of oxidative stress.Keeping SO2 of cultured erythrocytes in vitro at the states of 0.3,0.5,0.7,0.9and 0.98,respectively,we induced oxidative stress by tert-buthylhydroperoxide（BHP,0.15mmol/L of final concentration）.After incubation,antioxidant capacity was assessed by measuring content of reduced glutathin hormone（GSH） in erythrocytes.Methemoglobin（MetHb） content,lipid peroxidation（thiobarbituric acid-reactive substances,TBARS） and denatured globin-chains on the plasma membrane were measured to assess the extent of oxidative damages.The results showed that in the presence of BHP,GSH contents increased from 0.3 to 0.98 groups;MetHb,TBARS and globin-chains levels all dropped with the rise of SO2.In conclusion,antioxidant capacity and oxidative damages of erythrocytes are closely related to SO2,declined SO2 could promote oxidative damages of erythrocytes.

关 键 词：氧化损伤 红细胞 血氧饱和度 

分 类 号：R329[医药卫生—人体解剖和组织胚胎学]