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钒介导的NADH氧化作用会因铝而增强,并受到维生素E和某些铜(II)配合物的抑制。

Vanadium-mediated oxidation of NADH is enhanced by aluminium and inhibited by vitamin E and some copper (II) complexes.

作者信息

Abou-Seif M A

机构信息

Chemistry Department, Faculty of Science, Mansoura University, Egypt.

出版信息

Ann Clin Biochem. 1997 Nov;34 ( Pt 6):645-50. doi: 10.1177/000456329703400608.

DOI:10.1177/000456329703400608
PMID:9367002
Abstract

The effect of aluminium on vanadium-mediated oxidation of NADH was examined. The oxidation of NADH was enhanced in the presence of aluminium. The effect was concentration dependent. Vitamin E and copper (II) complexes with superoxide dismutase (SOD)-like activities containing isobutyric acid hydrazine were tested for their effect on the vanadium-mediated oxidation of NADH. The stimulatory effect of aluminium was decreased upon addition of different concentrations of vitamin E and copper (II) complexes. These results indicate that the biological toxicity of aluminium may be attributed to its enhancement of the production of superoxide radicals (O2.-) in association with the accumulation of other trace elements such as vanadium.

摘要

研究了铝对钒介导的NADH氧化的影响。在铝存在的情况下,NADH的氧化增强。该效应具有浓度依赖性。测试了维生素E以及具有类超氧化物歧化酶(SOD)活性的含异丁酸肼的铜(II)配合物对钒介导的NADH氧化的影响。添加不同浓度的维生素E和铜(II)配合物后,铝的刺激作用减弱。这些结果表明,铝的生物毒性可能归因于其与钒等其他微量元素的积累相关联,增强了超氧自由基(O2.-)的产生。

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