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41.
以1,1'-二甲基二茂铁(DMFc)作为葡萄糖氧化酶的电子传递体,用聚合物Nafion把DMFc及葡萄糖氧化酶固定在玻碳电极上,然后在电极上修饰一层Nafion膜,制备成葡萄糖传感器.探讨了温度、pH值、扫描速度及工作电位对催化电流的影响.该传感器具有抗干扰能力强、响应快等特点,它的线性范围为5.0×10-4~1.5×10-2mol/L,响应时间小于30s. 相似文献
42.
用膜透析技术和静息细胞系统,对影响葡萄糖氧化酶(GOD)发酵的控制因素进行了研究。静息细胞系统显示:鸟氨酸、谷氨酸、甘氨酸、丙氨酸、丝氨酸和胱氨酸等氨基酸对GOD的合成有促进作用;葡萄糖酸和丙酮酸对GOD的合成有阻遏作用,1.5mmol/L的丙酮酸使酶活降低46.24%;20mmol/L的葡萄糖酸使酶活降低21%左右,但葡萄糖酸浓度增大,有被菌体作为碳源利用的可能。利用膜透析技术可除去部分发酵过程中产生的葡萄糖酸和丙酮酸等阻遏物,减少它们对GOD合成的分解代谢物的阻遏作用,与分批发酵相比.提高酶活40%左右。 相似文献
43.
乙醇酸氧化酶研究进展 总被引:7,自引:0,他引:7
徐杰 《华南师范大学学报(自然科学版)》2002,(3):106-111
概述乙醇酸氧化酶研究存在的问题和进展,指出乙醇酸氧化酶被认为只含单种亚基,但该观点难于解释不同植物乙醇酸氧化酶为何等电点(pI)相差较大。首次介绍乙醇酸氧化酶 是种至少有GOI(pI≈7.4)、GOⅡ(pI≈9.4)和GOⅢ(pI≈8.3)的同工酶,以及GOⅠ只含单种亚基,GOⅡ和GOⅢ则可能含两种亚基的新观点。 相似文献
44.
Y. Nagata 《Cellular and molecular life sciences : CMLS》1992,48(8):753-755
The physiological role of D-amino acid oxidase (EC 1. 4. 3. 3) in mouse brain is described. The presence of D-enantiomers of neutral common amino acids was surveyed in the brain. D-serine was shown to be present at high concentration only in regions where the enzyme activity was low. In normal mice whose D-amino acid oxidase activity was much higher in the cerebellum than in the cerebrum, free D-serine content was apparently lower in the cerebellum than in the cerebrum. In mice of a mutant strain lacking D-amino acid-oxidase activity, the free D-serine level was remarkably high both in the cerebrum and cerebellum. The results suggest that the enzyme is involved in the elimination of free D-serine in the cerebellum. 相似文献
45.
用谷氨酸氧化酶测试液浸湿白卷纸置于菌落上,根据白卷纸上显示红色快慢、深浅,就能大致测得该菌落菌株产酶能力高低。该法可靠性大、工作量小、操作简便,显示结果快。利用该法,配合亚硝酸诱变,在短暂三个月内,将L-谷氨酸氧化酶产生菌株产酶能力提高了约25倍。 相似文献
46.
用微铂盘电极和交联法制得的酶膜构成葡萄糖酶电极,测定其电流响应特性,研究了酶的固定化条件:酶含量以及载体蛋白和交联剂的用量等,对响应特性的影响。提出较适宜的酶电极制备方法,并检测了所得的电极在不同pH溶液中的灵敏度,指出其最佳操作条件。 相似文献
47.
48.
Ferioli ME Bottone MG Soldani C Pellicciari C 《Cellular and molecular life sciences : CMLS》2004,61(21):2767-2773
The suggestion has been made that polyamines may be involved in the control of cell death, since exceedingly high or low levels induce apoptosis in different cell systems. For a deeper insight into the relationship between apoptosis and polyamine metabolism, we investigated in vitro the effect on rat thymocytes of mitoguazone (MGBG, which inhibits S-adenosylmethionine decarboxylase, i.e. a key enzyme in the polyamine biosynthetic pathway). Thymocytes were selected as an especially suitable model system, since they undergo spontaneous apoptosis in vivo and can be easily induced to apoptose in vitro by etoposide, used here as an apoptogenic agent. MGBG protected thymocytes from both spontaneous and drug-induced apoptosis, and this protective effect was associated with a decrease in polyamine oxidase activity and total polyamine levels.Received 7 July 2004; received after revision 2 September 2004; accepted 9 September 2004 相似文献
49.
Alternative splicing of Bcl-2-related genes: functional consequences and potential therapeutic applications 总被引:6,自引:0,他引:6
Apoptosis is a morphologically distinct form of cell death. It is executed and regulated by several groups of proteins. Bcl-2 family proteins are the main regulators of the apoptotic process acting either to inhibit or promote it. More than 20 members of the family have been identified so far and most have two or more isoforms. Alternative splicing is one of the major mechanisms providing proteomic complexity and functional diversification of the Bcl-2 family proteins. Pro- and anti-apoptotic Bcl-2 family members should function in harmony for the regulation of the apoptosis machinery, and their relative levels are critical for cell fate. Any mechanism breaking down this harmony by changing the relative levels of these antagonistic proteins could contribute to many diseases, including cancer and neurodegenerative disorders. Recent studies have shown that manipulation of the alternative splicing mechanisms could provide an opportunity to restore the proper balance of these regulator proteins. This review summarises current knowledge on the alternative splicing products of Bcl-2-related genes and modulation of splicing mechanisms as a potential therapeutic approach.Received 5 January 2004; received after revision 31 March 2004; accepted 6 April 2004 相似文献
50.
The superoxide-generating NADPH oxidase: structural aspects and activation mechanism 总被引:31,自引:0,他引:31
Vignais PV 《Cellular and molecular life sciences : CMLS》2002,59(9):1428-1459
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 相似文献