佛波酯心脏毒性：是否涉及超氧阴离子自由基？
Phorbol ester cardiotoxicity: are .O2-radicals involved?
作者信息
Esser E, Loschen G, Flohé L
机构信息
Grünenthal GmbH, Center of Research, Aachen.
出版信息
Arch Toxicol. 1991;65(4):335-9. doi: 10.1007/BF01968969.
The effect of superoxide dismutase (SOD) on cardiotoxic effects induced by phorbol 12-myristate 13-acetate (PMA) was investigated in isolated perfused rat hearts. The negative inotropic effect, vasoconstriction, and mild bradycardia were uneffected by SOD in the perfusion medium. Perfusion of Langendorff hearts with PMA and oxidized cytochrome c +/- SOD gave no evidence for a formation of .O2 radicals in response to PMA. Cytochrome c reduction detected in the perfusate of PMA-treated Langendorff hearts is not inhibited by SOD and has thus to be attributed to .O2-independent myocardial reducing systems.
在离体灌注大鼠心脏中研究了超氧化物歧化酶（SOD）对佛波酯12-肉豆蔻酸酯13-乙酸酯（PMA）诱导的心脏毒性作用的影响。灌注介质中的SOD对负性肌力作用、血管收缩和轻度心动过缓无影响。用PMA和氧化型细胞色素c+/-SOD灌注Langendorff心脏，未发现有因PMA而形成超氧阴离子自由基的证据。在PMA处理的Langendorff心脏灌注液中检测到的细胞色素c还原不受SOD抑制，因此应归因于不依赖超氧阴离子的心肌还原系统。
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