Conjugated dienes (CD) and thiobarbituric acid reactive substances (TBARS) have been estimated during the autoperoxidation of chromatographically pure phosphatidylcholine from hen eggs (EYPC) in multilamellar liposomes by UV-VIS spectrophotometry. During the propagation phase of autoperoxidation reaction, n-decane (C10) and n-octadecane (C18) gradually inhibit EYPC peroxidation up to 0:2:1 and 1:1 alkane:EYPC molar ratios, respectively. At higher molar ratios, the yield of estimated autoperoxidation products increases. At the highest molar ratio studied (alkane:EYPC = 2:1), the CD and TBARS concentrations exceed their levels in control sample without alkane added. The changes in the lipid bilayer thickness estimated from the small-angle neutron scattering (SANS) curves of unilamellar dioleoylphosphatidylcholine (DOPC) liposomes have indicated that C10 is located in the bilayer hydrophobic region parallel to the DOPC acyl chains at low molar ratios (C10:DOPC < or = 0.4). At higher molar ratios (0.6 < or = C10:DOPC < or = 1.0), the alkane changes its location into the center of the bilayer between the apposing monolayers. The alkane location parallel to polyunsaturated lipid fatty acyl chains RH separates these chains resulting in a decreased frequency of their encounters, in decreased yields of ROO. + RH-->ROOH + R., 2 ROOH-->RO. + ROO. + H2O and RO. + RH-->R. + ROH free radical reactions, and consequently, in decreased autoperoxidation. Autoperoxidation returns to the control values due to alkane redistribution into the bilayer center. 1H decoupled 31P NMR spectra of EYPC + C10 aqueous dispersions have shown that the lipid bilayer transforms into nonbilayer phases at C10:EYPC > 1:1 molar ratios. The inverted hexagonal HII phase with C10 (or C18) preferentially located in the interstitial regions of the HII unit cell displays higher autoperoxidation than the control bilayer sample due to greater motional freedom of RH chains in the HII phase.