Oxidative stress is a state of imbalance between reactive oxygen species (ROS), and the ability of the organism to defend against them, leading to progressive oxidative damage. ROS causes oxidation of proteins, DNA and lipids, which may cause direct tissue injury or induce a variety of cellular responses. Low-density lipoprotein (LDL) lipid peroxidation is one of the markers for oxidative stress. This study aimed to determine the mainstream cigarette smoke constituents that participate in LDL lipid peroxidation in in vitro experiments.Effect of gas vapour phase-bubbled phosphate buffered saline (GVP-PBS) on LDL lipid peroxidation was estimated to account for approximately 80 percent of the effect of whole smoke-bubbled PBS (WS-PBS) in the experiment with a reference cigarette, 3R4F. Also, benzo[a]pyrene, phenols in the particulate phase (PP) and carbonyls in GVP were implied as inducers of LDL lipid peroxidation by correlative analysis using 9 different sample cigarettes. Exposure to each of benzo[a]pyrene or phenol compounds in the amount equivalent to that in WS-PBS of 3R4F revealed none of the compounds induced LDL lipid peroxidation. However, the effect of a mixture of phenols on LDL lipid peroxidation was estimated to account for only about 3 percent of the effect of WS. Of the carbonyls tested, only acrolein induced LDL lipid peroxidation at almost 1.5 times in comparison with the effect of WS. Effect of GVP-PBS with acrolein in the amount equivalent to that in WS-PBS of 3R4F was less than the sum of the individual effect of GVP-PBS and acrolein.In conclusion, GVP is more involved in the induction of LDL lipid peroxidation than PP. And, acrolein accounts for much of the effect of GVP on LDL lipid peroxidation, and its effect could be suppressed by other chemical components.