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肌红蛋白的自动氧化机制。

The mechanism of autooxidation of myoglobin.

作者信息

Brantley R E, Smerdon S J, Wilkinson A J, Singleton E W, Olson J S

机构信息

Department of Biochemistry and Cell Biology, Rice University, Houston, Texas 77251.

出版信息

J Biol Chem. 1993 Apr 5;268(10):6995-7010.

PMID:8463233
Abstract

Time courses for the autooxidation of native and mutant sperm whale and pig myoglobins were measured at 37 degrees C in the presence of catalase and superoxide dismutase. In sperm whale myoglobin, His64(E7) was replaced with Gln, Gly, Ala, Val, Thr, Leu, and Phe; Val68(E11) was replaced with Ala, Ile, Leu, and Phe; Leu29(B10) was replaced with Ala, Val, and Phe. In pig myoglobin, His64(E7) was replaced with Val; Val68(E11) was replaced with Thr and Ser; Thr67(E10) was replaced with Ala, Val, Glu, and Arg; Lys45(CD3) was replaced with Ser, Glu, His, and Arg. The observed pseudo-first order rate constants varied over 4 orders of magnitude, from 58 h-1 (H64A) to 0.055 h-1 (native) to 0.005 h-1 (L29F) at 37 degrees C, pH 7, in air. The dependences of the observed autooxidation rate constant on oxygen concentration and pH were measured for native and selected mutant myoglobins. In the native proteins and in most mutants still possessing the distal histidine, autooxidation occurs through a combination of two mechanisms. At high [O2], direct dissociation of the neutral superoxide radical (HO2) from oxymyoglobin dominates, and this process is accelerated by decreasing pH. At low [O2], autooxidation occurs by a bimolecular reaction between molecular oxygen and deoxymyoglobin containing a weakly coordinated water molecule. The neutral side chain of the distal histidine (His64) inhibits autooxidation by hydrogen bonding to bound oxygen, preventing both HO2 dissociation and the oxidative bimolecular reaction with deoxymyoglobin. Replacement of His64 by amino acids incapable of hydrogen bonding to the bound ligand markedly increases the rate of autooxidation and causes the superoxide mechanism to predominate. Increasing the polarity of the distal pocket by substitution of Val68 with Ser and Thr accelerates autooxidation, presumably by facilitating protonation of the Fe(II).O2 complex. Increasing the net anionic charge at the protein surface in the vicinity of the heme group also enhances the rate of autooxidation. Decreasing the volume of the distal pocket by replacing small amino acids with larger aliphatic or aromatic residues at positions 68 (E11) and 29 (B10) inhibits autooxidation markedly by decreasing the accessibility of the iron atom to solvent water molecules.

摘要

在37℃、过氧化氢酶和超氧化物歧化酶存在的条件下,测定了天然型和突变型抹香鲸肌红蛋白及猪肌红蛋白的自动氧化时间进程。在抹香鲸肌红蛋白中,His64(E7)被替换为Gln、Gly、Ala、Val、Thr、Leu和Phe;Val68(E11)被替换为Ala、Ile、Leu和Phe;Leu29(B10)被替换为Ala、Val和Phe。在猪肌红蛋白中,His64(E7)被替换为Val;Val68(E11)被替换为Thr和Ser;Thr67(E10)被替换为Ala、Val、Glu和Arg;Lys45(CD3)被替换为Ser、Glu、His和Arg。在37℃、pH 7、空气中,观察到的准一级反应速率常数变化超过4个数量级,从58 h⁻¹(H64A)到0.055 h⁻¹(天然型)再到0.005 h⁻¹(L29F)。测定了天然型和选定突变型肌红蛋白的自动氧化速率常数对氧浓度和pH的依赖性。在天然蛋白以及大多数仍保留远端组氨酸的突变体中,自动氧化通过两种机制共同发生。在高[O₂]时,中性超氧自由基(HO₂)从氧合肌红蛋白的直接解离占主导,并且该过程通过降低pH而加速。在低[O₂]时,自动氧化通过分子氧与含有弱配位水分子的脱氧肌红蛋白之间的双分子反应发生。远端组氨酸(His64)的中性侧链通过与结合氧形成氢键来抑制自动氧化,从而防止HO₂解离以及与脱氧肌红蛋白的氧化双分子反应。用不能与结合配体形成氢键的氨基酸替换His64会显著增加自动氧化速率,并使超氧机制占主导。用Ser和Thr替换Val68增加远端口袋的极性会加速自动氧化,可能是通过促进Fe(II).O₂复合物的质子化。在血红素基团附近的蛋白质表面增加净阴离子电荷也会提高自动氧化速率。通过在68(E11)和29(B10)位用较大的脂肪族或芳香族残基替换小氨基酸来减小远端口袋的体积,会通过降低铁原子与溶剂水分子的可及性而显著抑制自动氧化。

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