Puppo A, Cecchini R, Aruoma O I, Bolli R, Halliwell B
Laboratoire de Biologie Végètale, Université de Nice, France.
Free Radic Res Commun. 1990;10(6):371-81. doi: 10.3109/10715769009149906.
Mercaptopropionylglycine (MPG) has a marked cardioprotective action in several model systems of ischaemia-reoxygenation injury. Suggested mechanisms of action include scavenging of hydroxyl radical and of hypochlorous acid and reacting with an oxidant formed by reaction of myoglobin with H2O2, thereby slowing lipid peroxidation stimulated by myoglobin-H2O2 mixtures. This oxidant seems not to be singlet O2 or hydroxyl radical. Studies in vitro show that scavenging of hypochlorous acid is a feasible mechanism of cardioprotective action for MPG in vivo in ischaemia/reperfusion systems to which neutrophil-mediated injury contributes. However, the poor ability of MPG to inhibit lipid peroxidation stimulated by myoglobin/H2O2 mixtures and its ability to increase iron ion release from myoglobin in the presence of a large excess of H2O2 suggests that MPG is unlikely to protect the myocardium by interfering with oxidants produced by the myoglobin-H2O2 system.
巯基丙酰甘氨酸(MPG)在多种缺血 - 再灌注损伤模型系统中具有显著的心脏保护作用。其作用机制包括清除羟自由基和次氯酸,并与肌红蛋白与过氧化氢反应形成的氧化剂发生反应,从而减缓肌红蛋白 - 过氧化氢混合物刺激的脂质过氧化。这种氧化剂似乎不是单线态氧或羟自由基。体外研究表明,在中性粒细胞介导的损伤起作用的缺血/再灌注系统中,清除次氯酸是MPG在体内发挥心脏保护作用的一种可行机制。然而,MPG抑制肌红蛋白/过氧化氢混合物刺激的脂质过氧化的能力较差,且在大量过氧化氢存在的情况下它能增加肌红蛋白中铁离子的释放,这表明MPG不太可能通过干扰肌红蛋白 - 过氧化氢系统产生的氧化剂来保护心肌。