Abudu Ntei, Miller James J, Attaelmannan Mohammed, Levinson Stanley S
Department of Pathology and Laboratory Medicine, University of Louisville, 40292, Louisville, KY, USA.
Clin Chim Acta. 2004 Jan;339(1-2):11-25. doi: 10.1016/j.cccn.2003.09.018.
This review focuses on the process of arteriosclerosis arising from oxidative stress on lipoproteins and the general failure of randomized human trials using vitamins to retard this process.
As well as clinical trials, the paper reviews the mechanisms by which a variety of oxidants act. Antioxidants are discussed, emphasizing interactions of vitamins C and E with transition metals that can lead to prooxidation. There is a focus on interactions between supplemental or co-antioxidants that counterbalance prooxidant effects of one another.
It is concluded that normal cellular supplementation mechanisms are poorly accessible in the arteriosclerotic plaque leading to a prooxidant environment in which the haphazard introduction of vitamins could potentially be hazardous. Continued investigations into basic and clinical redox interactions of the kind discussed in this review using new measuring techniques may lead to approaches whereby antioxidants can be introduced into tissue in controlled ways for reducing arteriosclerosis.
本综述聚焦于脂蛋白氧化应激引发动脉粥样硬化的过程,以及使用维生素延缓该过程的随机人体试验总体失败的情况。
除临床试验外,本文还回顾了多种氧化剂的作用机制。文中讨论了抗氧化剂,重点强调了维生素C和E与过渡金属的相互作用,这种相互作用可能导致促氧化作用。文中关注了补充性抗氧化剂或协同抗氧化剂之间的相互作用,这些抗氧化剂可相互抵消促氧化作用。
得出的结论是,在动脉粥样硬化斑块中,正常的细胞补充机制难以发挥作用,从而导致促氧化环境,在这种环境中随意引入维生素可能具有潜在危害。使用新的测量技术对本综述中所讨论的这类基础和临床氧化还原相互作用进行持续研究,可能会带来一些方法,通过这些方法可以以可控的方式将抗氧化剂引入组织,以减轻动脉粥样硬化。