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Second hand smoke exposure mediates oxidative modification of plasma apolipoprotein E

The objective of our study was to assess if second hand smoke exposure predisposes subjects towards developing heart disease. We monitored the effect of reactive aldehydes in tobacco smoke on the status of plasma apolipoprotein E (apoE). ApoE plays a critical role in regulating plasma cholesterol homeostasis, since it serves as a ligand for the low density lipoprotein family of receptors. ELISA indicated that rats exposed to low doses of tobacco smoke had lower plasma apoE levels compared to the control group. Immunoprecipitation analysis revealed that the smoke‐exposed group also had higher levels of modified apoE in their lipid‐free fractions. There were no differences between the two groups in lipid peroxidation products levels or in the susceptibility of the lipoproteins to lipid peroxidation. In vitro analysis using recombinant apoE provided further support for modification of essential lysines. Our results suggest that the occurrence of oxidatively modified apoE in a lipid‐free state can result in decreased clearance of plasma lipoproteins. We propose that sustained second hand smoke exposure can potentially lead to a proatherogenic profile. Source of research support: Tobacco Related Disease Research Program, American Heart Association, NIH R25 HL096365‐01, CSULB funding and SCAC award.