Rabovsky Alexander B, Buettner Garry R, Fink Bruno
Research & Development, Melaleuca Inc, 4609 West 65th South, Idaho Falls, ID 83402, USA.
Free Radical and Radiation Biology, The University of Iowa, Iowa City, IA, USA.
BMC Nutr. 2015 Dec;1. doi: 10.1186/s40795-015-0025-7. Epub 2015 Nov 14.
Redox active minerals in dietary supplements can catalyze unwanted and potentially harmful oxidations.
To determine if this occurs in vivo we employed electron paramagnetic (EPR) imaging. We used 1-hydroxy-3-carboxy-2,2,5,5-tetramethylpyrrolidine (CPH) as a reporter for one-electron oxidations, . free radical-mediated oxidations; the one-electron oxidation product of CPH, 3-carboxy-2,2,5,5-tetramethyl-1-pyrrolidinyloxy (CP), is a nitroxide free radical that is relatively persistent in vivo and detectable by EPR. As model systems, we used research formulations of vitamin mineral supplements (RVM) that are typical of commercial products.
In in vitro experiments, upon suspension of RVM in aqueous solution, we observed: (1) the uptake of oxygen in the solution, consistent with oxidation of the components in the RVM; (2) the ascorbate free radical, a real-time indicator of ongoing oxidations; and (3) when amino acid/oligosaccharide (AAOS; glycinate or aspartate with non-digestible oligofructose) served as the matrix in the RVM, the rate of oxidation was significantly slowed. In a murine model, EPR imaging showed that the ingestion of RVM along with CPH results in the one-electron oxidation of CPH by RVM in the digestive system. The resulting CP distributes throughout the body. Inclusion of AAOS in the RVM formulation diminished the oxidation of CPH to CP in vivo.
These data demonstrate that typical formulations of multivitamin/multimineral dietary supplements can initiate the oxidation of bystander substances and that AAOS-complexes of essential redox active metals, . copper and iron, have reduced ability to catalyze free radical formation and associated detrimental oxidations when a part of a multivitamin/multimineral formulation.
膳食补充剂中的氧化还原活性矿物质可催化不必要的且可能有害的氧化反应。
为确定这种情况是否在体内发生,我们采用了电子顺磁共振(EPR)成像技术。我们使用1-羟基-3-羧基-2,2,5,5-四甲基吡咯烷(CPH)作为单电子氧化反应的报告分子,即自由基介导的氧化反应;CPH的单电子氧化产物3-羧基-2,2,5,5-四甲基-1-吡咯烷氧基(CP)是一种氮氧自由基,在体内相对稳定且可通过EPR检测到。作为模型系统,我们使用了商业产品中常见的维生素矿物质补充剂(RVM)研究配方。
在体外实验中,将RVM悬浮于水溶液后,我们观察到:(1)溶液中氧气的摄取,这与RVM中成分的氧化一致;(2)抗坏血酸自由基,这是正在进行的氧化反应的实时指标;(3)当氨基酸/低聚糖(AAOS;甘氨酸盐或天冬氨酸盐与不可消化的低聚果糖)作为RVM中的基质时,氧化速率显著减慢。在小鼠模型中,EPR成像显示,摄入RVM和CPH会导致RVM在消化系统中使CPH发生单电子氧化。生成的CP分布于全身。在RVM配方中加入AAOS可减少体内CPH氧化为CP的反应。
这些数据表明,多种维生素/多种矿物质膳食补充剂的典型配方可引发旁观者物质的氧化,并且当作为多种维生素/多种矿物质配方的一部分时,必需的氧化还原活性金属(如铜和铁)的AAOS复合物催化自由基形成及相关有害氧化反应的能力降低。