Chen C, Loo G
Department of Food, Nutrition and Food Service Management, School of Human Environmental Sciences, University of North Carolina at Greensboro 27412-5001, USA.
Atherosclerosis. 1995 Jan 20;112(2):177-85. doi: 10.1016/0021-9150(94)05412-c.
Oxidative modification of low density lipoprotein (LDL) by cigarette smoke has been suggested in several recent studies. To characterize possible modification of LDL by cigarette smoke extract (CSE), we incubated LDL with CSE either in the presence or absence of the chemical pro-oxidants, cupric chloride or 2,2'-azo-bis(2-amidinopropane) hydrochloride (AAPH). Surprisingly, CSE inhibited oxidative modification of LDL induced by either copper or AAPH. Under such oxidant stress conditions, CSE inhibited formation of thiobarbituric acid-reactive substances and also inhibited the increased agarose gel electrophoretic mobility of LDL in a dose-response manner. In addition, CSE prevented degradation of phosphatidylcholine to lysophosphatidylcholine and also fragmentation of the apolipoprotein B-100 moiety of LDL. Finally, CSE inhibited loss of immunoreactivity of the treated LDL with a murine monoclonal antibody against human apolipoprotein B-100. On the other hand, at higher concentrations, CSE per se was still able to cause structural changes in LDL. After incubation with CSE for 24 h, LDL showed a slight increase in agarose gel electrophoretic mobility, a slight loss of immunoreactivity with monoclonal antibody, and a marked increase in protein carbonyl formation. Lipid peroxidation did not appear to be involved in the modification of LDL caused by CSE. It is suggested that reactive aldehydes present in cigarette smoke may cause direct chemical modification of LDL. Furthermore, the free radical-scavenging potential of the tar fraction of cigarette smoke may be responsible for the apparent antioxidant properties of CSE against LDL oxidation.
