Ko K M, Godin D V
Department of Pharmacology & Therapeutics, Faculty of Medicine, University of British Columbia, Vancouver, Canada.
Mol Cell Biochem. 1991 Feb 27;101(1):23-9. doi: 10.1007/BF00238434.
Phytic acid stimulated the myoglobin-t-butylhydroperoxide (TBHP)-catalysed oxidation of uric acid, but inhibited the peroxidation of erythrocyte membrane lipids induced by the same system. Butylated hydroxytoluene, a free radical chain reaction-terminating antioxidant, also suppressed the myoglobin-TBHP-induced lipid peroxidation. Moreover, phytic acid inhibited the hydroxyl radical-induced degradation of deoxyribose, but the extent of inhibition in this system was reduced by increasing the ferric ion concentration, suggesting that these effects of phytic acid on the myoglobin-TBHP-mediated oxidation are more likely attributable to its metal chelating properties rather than to a free radical scavenging action. The effectiveness of phytic acid, a naturally occurring antioxidant, in the inhibition of both iron- (as previously shown) and myoglobin-dependent lipid peroxidation suggests its possible therapeutic application as a non-toxic antioxidant for ameliorating the extent of oxy-radical-mediated myocardial ischemia/reperfusion damage.
植酸刺激了肌红蛋白-叔丁基过氧化氢(TBHP)催化的尿酸氧化,但抑制了同一系统诱导的红细胞膜脂质过氧化。丁基化羟基甲苯,一种终止自由基链反应的抗氧化剂,也抑制了肌红蛋白-TBHP诱导的脂质过氧化。此外,植酸抑制了羟基自由基诱导的脱氧核糖降解,但在该系统中,通过增加铁离子浓度,抑制程度降低,这表明植酸对肌红蛋白-TBHP介导的氧化的这些作用更可能归因于其金属螯合特性,而非自由基清除作用。植酸,一种天然存在的抗氧化剂,在抑制铁(如先前所示)和肌红蛋白依赖性脂质过氧化方面的有效性表明,它作为一种无毒抗氧化剂,在减轻氧自由基介导的心肌缺血/再灌注损伤程度方面可能具有治疗应用价值。