阿霉素中毒心肌细胞脂质过氧化及其导致的钙超负荷的研究  

Study on the lipid peroxidation and subsequent Ca 2+ overloading with in the doxorubicin toxic cardial cells

作　　者：张亚臣[1] 荣烨之[1] 赵美华[1] 吕宝经[1] 张懋贞[1] 黄国芳[1] 杨瑾文[1] 

机构地区：[1]上海第二医科大学附属新华医院心内科

出　　处：《中国病理生理杂志》1998年第6期688-691,共4页Chinese Journal of Pathophysiology

摘　　要：目的和方法：通过测定心肌细胞脂质过氧化水平及细胞内钙离子浓度，探讨了阿霉素中毒心肌细胞损伤机制与脂质过氧化及钙离子超负荷的关系。结果：中毒心肌细胞培养基中ＬＤＨ释放量由２５０．２增加到８５３．７μｍｏｌ／Ｌ，ＳＯＤ活力由２５７．５５（Ｕ／ｍｇ·ｐｒｏ）下降到１８５．８８（Ｕ／ｍｇ·ｐｒｏ），丙二醛（ＭＤＡ）含量由１．４０９（ｎｍｏｌ／ｍｇ·ｐｒｏ）增加到１．６３８（ｎｍｏｌ／ｍｇ·ｐｒｏ），细胞内游离钙浓度由２４０．１８（ｎｍｏｌ／Ｌ）增加到１４６０．４０（ｎｍｏｌ／Ｌ）；阿霉素中毒早期仅有〔Ｃａ２＋〕ｉ升高；中毒４ｈ后出现脂质过氧化、心肌损伤加重及〔Ｃａ２＋〕ｉ的进一步升高；结论：心肌细胞内〔Ｃａ２＋〕ｉ早期增高是心肌损伤的始动环节。Abstract AIM and METHOD:To explore the pathogenesis of lipid peroxidation and subsequent Ca 2+ overloading in the doxorubicin toxic myocardial cells. RESULTS:The LDH in the culture medium was increased (from 250.2 to 853.7 μmol/L), SOD was decreased (from 257.55 to 185.88 μmol/L), MDA content in plasma was increased (from 1.409 to 1.640 nmol/mg pro) and calcium concentration was increased (from 240.18 to 1460.40 nmol/L) in doxorubicin toxic myocardial cells. In the early stage, only calcium concentration increased; lipid peroxidation and further calcium overloading was observed in the myocardial cells after doxorubicin incubated for 4 hours. CONCLUSION:Myocardial cell damage was due to calcium overloading, lipid peroxidation and further Ca 2+ overloading induced by the lipid peroxidation were the fundamental pathogenesis. MeSH Doxorubicin; Myocardium; Lipid peroxides; Calcium

关 键 词：阿霉素 钙 药物中毒 脂质过氧化 心肌细胞 

分 类 号：R542.202[医药卫生—心血管疾病] R595.4[医药卫生—内科学]