Hogg N, Rice-Evans C, Darley-Usmar V, Wilson M T, Paganga G, Bourne L
Division of Biochemistry, UMDS-Guy's Hospital, London, UK.
Arch Biochem Biophys. 1994 Oct;314(1):39-44. doi: 10.1006/abbi.1994.1409.
It has previously been reported that mb in both the iron-oxo ferryl and the ferric oxidation states can promote lipid peroxidation and lead to oxidative modification of low-density lipoprotein. The mechanism of these oxidation reactions is unclear and could involve either lipid hydroperoxide-dependent or independent reactions. In order to ascertain which of the afore-mentioned mechanisms predominates, the effects of exogenous lipid hydroperoxides on the ability of Mb, in its various oxidation states, to oxidize low-density lipoprotein has been investigated. The results suggest that oxidation proceeds through a one-electron redox cycle between met and ferryl myoglobin and that the reactions of both redox forms are at least partially dependent on lipid hydroperoxides within the LDL particle.
此前已有报道称,处于铁氧代高铁血红素和三价铁氧化态的肌红蛋白均可促进脂质过氧化,并导致低密度脂蛋白的氧化修饰。这些氧化反应的机制尚不清楚,可能涉及脂质氢过氧化物依赖性或非依赖性反应。为了确定上述哪种机制占主导地位,研究了外源脂质氢过氧化物对处于各种氧化态的肌红蛋白氧化低密度脂蛋白能力的影响。结果表明,氧化过程通过高铁肌红蛋白和铁氧代肌红蛋白之间的单电子氧化还原循环进行,并且两种氧化还原形式的反应至少部分依赖于低密度脂蛋白颗粒内的脂质氢过氧化物。