摘要
目的 :探讨超氧阴离子自由基 (O2 ·- )对培养心肌细胞的影响。方法 :利用黄嘌呤氧化酶 /黄嘌呤(XO/X)产生O2 ·- 系统作用于原代培养的新生大鼠心肌细胞 ,观察其对心肌细胞的损伤 ,并分析其对核DNA、Na/K ATP酶 (ATPase)活性和脂质过氧化的影响。结果 :O2 ·- 使心肌细胞受损 ,扫描电镜见细胞伪足变短甚或消失并趋于固缩 ,乳酸脱氢酶漏出增多〔(2 0 2 .0 0± 19.5 0 )U/L〕 ,核DNA单链断裂增加 (DNA EB的相对荧光强度 :31.93± 3.4 7) ,ATPase活性下降 [4 .75± 0 .4 3(μmol/min) a],丙二醛含量增加〔(1.16± 0 .14 )nmol/L〕 ,过氧化氢酶 (CAT)能明显抑制这些损伤效应。结论 :O2 ·- 可对心肌细胞及其核酸、蛋白质和脂质造成损伤。
Objective:To investigate the effects of the superoxide anionic radicals(O 2 ·- ) on the cultured cardiomyocytes of neonatal rat.Methods:Cytotoxity in cardiomyocytes was induced by O 2 ·- , which was produced by reactive system of xanthine oxidase/xanthine(XO/X). The morphologic changes in cardiomyocytes was examined by electron microscope,and the DNA-EB complex, content of LDH and MDA and ATPase activity were measured respectively.Results:The levels of LDH and MDA were significantly higher〔( 202.00 ± 19.50 ) U/L & ( 1.16 ± 0.14 ) nmol/L, respectively〕 in the cardiomyocytes exposed to O 2 ·- than those in control, with the concomitant growth inhibition of cardiomyocyte. The ATPase activity and fluorescence intensity of DNA EB complex decreased[ 4.75 ± 0.43 (μmol/min) a] and 31.93 ± 3.47 , respectively when O 2 ·- reacted with cardiomyocytes. Enough amount of catalase protected cardiomyocytes against O 2 ·- .Conclusion:It is suggested that O 2 ·- CQN can damage cardiomyocytes and its nucleic acids, proteins and lipids.
出处
《临床心血管病杂志》
CAS
CSCD
北大核心
2003年第7期410-412,共3页
Journal of Clinical Cardiology
关键词
超氧阴离子
心肌细胞
核酸
脂质
Superoxide anion
Cardiomyocyte
Nucleic acid
Lipid
