Oxidative Modification of Very Low Density Lipoprotein by Arterial Wall Cells

Modification of VLDL by arterial wall cells was observed. After incubating VLDL (200 &mgr;g protein/ml) with bovine aortic endothelial cells (EC), rabbit aortic smooth muscle cells (SMC) or mouse peritoneal macrophages (Mpsi)for 24 hours, the TBARS in VLDL increased strikingly to 7.80+/-O.75, 1O.6+/-O.90 and 11.4+/-O.70 nmol/mg-protein respectively, much higher than those of their controls (5.1O+/-0.60, 7.20+/-0.89, 5.30+/-O.54 nmol/mg-protein). The cell-modified VLDL migrated faster than the controls on agarose electrophoregram and the SDS-PAGE of the apolipoproteins showed that apo B(100) of VLDL was degraded to fragments without distinct bands, while apo E was essentially kept intact. Phosphatidylcholine was hydrolyzed to lysophosphatidylcholine during the modification process. These changes were inhibited by BHT, indicating that the modification of VLDL was an oxidative process. The result suggests that since VLDL could be oxidatively modified by arterial wall cells including EC, SMC, Mpsi in vitro, suggesting the oxidative modification of VLDL may occur in vivo and play an important role in atherogenesis.