Apo E-deficient mice which are highly atherogenic animals were used in order to study their plasma and lipoprotein lipid peroxidation in the absence or presence of oxidative stress. We have demonstrated that plasma from apo E knockout mice demonstrated increased lipid peroxidation both in the absence and in the presence of a free radical generating substance, 2,2-Azobis-(2-amidinopropane) hydrochloride (AAPH). Similarly, low and very low-density lipoprotein (LDL and VLDL) from apo E-deficient mice, but not their high-density lipoprotein (HDL), demonstrated increased lipid peroxidation. We suggest that in apo E-deficient mice, accelerated atherosclerosis is associated with increased lipid peroxidation of plasma, LDL and VLDL, as well as increased susceptibility of these lipoproteins to undergo lipid peroxidation under oxidative stress.