Dimethylsulphoxide (DMSO) promoted peroxidation in both linolenate and linoleate micelles. The promotional effect was most evident at concentrations of DMSO above 0.3 M with 0.012 M fatty acid. This was well above the DMSO concentration at which all the OH was scavenged by DMSO on the basis of the relative rate constants recorded. It was also found that DMSO did not decrease the yield of lipid hydroperoxide in a concentration range (0.01 to 0.1 M) where DMSO scavenges OH in competition with the unsaturated fatty acids. The sustaining mechanism could be accounted for in terms of CHsup(.)/sub 3/ and CH/sub 3/OOsup(.) being as effective as OH in initiating lipid peroxidation. A possible alternative explanation for the absence of protection by DMSO is that OH scavenging by DMSO is equivalent to lowering the dose-rate. The promotion of peroxidation at high DMSO concentration (> 1.0 M) was more difficult to account for, but may be analogous to the promotional effect of caesium and rubidium counterions.