Action of 1-(11-selenadodecyl)-glycerol and 1-(11-selenadodecyl)-3-trolox-glycerol against lipid peroxidation

Abstract

The antioxidant action on lipid peroxidation of the synthesized selenium compounds 1-(11-selenadodecyl)-glycerol (SeG) and 1-(11-selenadodecyl)-3-Trolox-glycerol (SeTrG, where Trolox = 6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid) was investigated. We compared the reactivity of the selenium compounds toward peroxyl radicals and their inhibitory effect on lipid peroxidation, induced by several kinds of initiating species such as azo compounds, metal ions, and superoxide/nitric oxide in solution, micelles, membranes, and rat plasma. SeTrG, but not SeG, scavenged peroxyl radicals. SeG reduced methyl linoleate hydroperoxides in organic solution and in methyl linoleate micelles oxidized by ferrous ion (Fe2+)/ascorbic acid. In rat plasma SeG and SeTrG decreased the formation of lipid hydroperoxides generated by hydrophilic azo compounds. SeG and SeTrG spared alpha-tocopherol (alpha-TOH) consumption in multilamellar vesicle membranes oxidized by hydrophilic or lipophilic initiators, and only SeTrG spared alpha-TOH in superoxide/nitric oxide oxidized membranes. In rat plasma oxidized by radical initiators (either hydrophilic or lipophilic) or superoxide/nitric oxide, SeTrG suppressed alpha-TOH consumption, but SeG had no effect. The two selenium-containing compounds showed inhibitory effects on lipid peroxidation that depended on their structure, the medium where they acted, and the oxidant used.