The extent of lipid peroxidation enhancement or inhibition by quinones in 3:1 egg‐yolk phosphatidylcholine (PC): linolenate (mol/mol) multilamellar vesicles, at pH 7.4, in the presence of Fe+2‐ascorbate, was measured. The para quinones 1,4‐benzoquinone (BQ), tetrafluorobenzoquinone (TFBQ), 1,4‐naphthoquinone (NQ), naphthoquinone‐2‐sulfonate (NQ2S), menadione (MNQ), naphthazarin (NZQ), quinizarin (QNZ), doxorubicin (DOXO) and daunomycin (DAUNO) were used in this work. These quinones comprise large ranges of octanol/buffer partition constants, one‐electron reduction potentials, and Fe+3 binding constants, as well as large differences in structure. All the quinones under study here inhibited the Fe+2‐ascorbate‐induced lipid peroxidation in the range of 2 to 6 mol % of quinone, relative to total lipid, with the exception of DOXO and DAUNO. The latter increase lipid peroxidation over that produced by Fe+2‐ascorbate alone. In general, no correlation was found between any of the quinone properties indicated above and the extent of lipid peroxidation inhibition/enhancement. However, for anthracycline‐type quinones (ATQs), i.e. NZQ, QNZ, DOXO and DAUNO, lipid peroxidation enhancements were observed only for the most hydrophilic ones, i.e. DOXO and DAUNO. Thus, the iron‐chelating feature of ATQs in conjunction with their moderate hydrophylicity are more important requisites for lipid peroxidation enhancement than other factors. The inhibitory effects of SOD, catalase and DFO on the lipid peroxidation extent of DOXO and DAUNO suggests that an anthracycline‐iron complex is responsible for the initiation of the peroxidation process by, presumably, reduction of hydrogen peroxide to produce a peroxidation initiator species. Less lipid peroxidation inhibition, or larger lipid peroxidation enhancement, is observed in the absence of ascorbate. The latter suggests that peroxidation inhibition, occurring in the presence of ascorbate, is caused by hydroquinone formation and the consequent phenol‐like antioxidant activity. The complete or partial insensitiveness of the lipid peroxidation process in the absence of ascorbate to SOD could also be explained by the lipid peroxidation enhancement through the lipid hydroperoxide reduction pathway mediated by the semiquinone, which is not competing against the hydroquinone‐induced inhibition.