盐胁迫对小麦耐盐突变体苗期超氧化物歧化酶活性的影响

对小麦盐突变体H8706－34，H8706－44，RH－48，RH8706－49室内水培的苗期（2叶小心），进行了0．7％的NaCl盐胁迫试验，结果表明，非盐胁迫时耐盐性强的突变体的超氧化物歧化酶（SOD）的活性极显著高于耐盐性差的突变体；在盐胁迫时，不同的突变体的SOD活性发生不同的变化，耐盐性强的突变体的SOD活性变化幅度较大，变化周期较长，表现出较好的适应性和对超氧自由基的反应能力；而耐盐性差的突变体的SOD活性的变化幅度小，且变化周期短，表现出较差的适应性和对超氧自由基的较的反应能力。     

牛血中SOD的提取技术研究

提出了以牛血为原料分离纯化SOD的方法 ,分离产率约为 6 0 % ,提纯倍数达 90 0倍 .与经典的J.M .McCord方法相比 ,该法不仅降低了制备成本、简化了工艺 ,而且其纯度和活力回收都有明显提高     

超氧化物歧化酶及其模拟研究

超氧化物歧化酶 (SOD)作为一种生物活性酶 ,在治疗由氧化应激所导致的疾病方面有着非常广阔的应用前景 .本文综述了国内外近年来有关 SOD的存在和结构、SOD活性的测定及模拟等方面的研究进展 .     

锰超氧化物歧化酶模型化合物的合成、表征及活性检测

研究近年来报道的有关锰超氧化物歧化酶及其活性部位的结构，以苹果酸，酒石酸与碳酸锰作用合成了两种超氧化物歧化酶的模型化合物，进行了红外、紫外谱图的表征，利用邻苯三酚自氧化法检测了它们的生物活性。     

一种新型超氧化物歧化酶的活性中心量子化学计算

借助Fe-SOD的晶体模型，运用Gaussian94程序包，采用HF下的LanL2DZ基组对一种新型的超氧化物歧化酶Ni-SOD的还原型Ni(Ⅱ）－SOD的活性中心进行了量子化学计算，由其分子轨道能量，电荷分布和前线轨道的贡献可以预见，Ni-SOD具有较高的结构稳定性和催化超氧离子的活性。     

钒模拟超氧化物歧化酶的活性中心计算

借助Fe-SOD的晶体结构模型，运用Gaussian 94程序包，采用HF下的LznL2DZ基组对钒辅基模拟超氧化物歧化酶的活性中心进行了量子化学计算，由其分子轨道能量，电荷分布和前线轨道的贡献可以理论预测，V－SOD具有较高的结构稳定性和催化超氧阴离子的活性。     

酵母菌SOD发酵条件的研究

研究环境条件对酵母菌SOD发酵的影响。试验结果表明,初糖浓度、金属离子、pH值、装液量和培养时间等对酵母发酵的生物量和SOD含量有较大影响。在初步优化发酵条件下,细胞生物量为33 90g L,菌体SOD含量为1871 68U L,发酵液产SOD能力为6 34×104U L。     

弱光照对螺旋藻抗氧化酶活性的影响

探讨了螺旋藻在弱光照下的抗氧化酶活力的变化。结果显示：在1100lx光照下，钝顶螺旋藻（Spirulina plentasis)314和极大螺旋藻（Spirulina maxima）438两者的SOD活性最低，黑暗条件下的活力分别是1100lx光照下的2．2倍和1．4倍；两者的APX则在600lx光照下，活星最大；两者的CAT的活性变化情况分别与各自的APX类似。     

胃液中超氧化物歧化酶与乳酸脱氢酶的相关性及其与膜系的关系

本文报道了胃癌胃液与非胃癌胃液中乳酸脱氢酶同功酶与超氧化物歧化酶的活性及其相关性。通过两种酶活性的比较得知,乳酸脱氢酶与超氧化物歧化酶的活性呈负相关。讨论了酶活性与癌细胞膜系损伤的关系。     

The superoxide-generating NADPH oxidase: structural aspects and activation mechanism

Flavocytochrome b ₅₅₈ is the catalytic core of the respiratory-burst oxidase, an enzyme complex that catalyzes the NADPH-dependent reduction of O₂ into the superoxide anion O₂ ^- in phagocytic cells. Flavocytochrome b ₅₅₈ is anchored in the plasma membrane. It is a heterodimer that consists of a large glycoprotein gp91phox (phox for phagocyte oxidase) (β subunit) and a small protein p22phox (α subunit). The other components of the respiratory-burst oxidase are water-soluble proteins of cytosolic origin, namely p67phox, p47phox, p40phox and Rac. Upon cell stimulation, they assemble with the membrane-bound flavocytochrome b ₅₅₈ which becomes activated and generates O₂ ^-. A defect in any of the genes encoding gp91phox, p22phox, p67phox or p47phox results in chronic granulomatous disease, a genetic disorder characterized by severe and recurrent infections, illustrating the role of O₂ ^- and the derived metabolites H₂O₂ and HOCl in host defense against invading microorganisms. The electron carriers, FAD and hemes b, and the binding site for NADPH are confined to the gp91phox subunit of flavocytochrome b ₅₅₈ . The p22phox subunit serves as a docking site for the cytosolic phox proteins. This review provides an overview of current knowledge on the structural organization of the O₂ ^--generating flavocytochrome b ₅₅₈ , its kinetics, its mechanism of activation and the regulation of its biosynthesis. Homologues of gp91phox, called Nox and Duox, are present in a large variety of non-phagocytic cells. They exhibit modest O₂ ^--generating oxidase activity, and some act as proton channels. Their role in various aspects of signal transduction is currently under investigation and is briefly discussed. Received 28 May 2002; received after revision 20 June 2002; accepted 24 June 2002