Low density lipoprotein (LDL) from male volunteers stimulated the thromboxane formation by human platelets.

LDL (0.5 - 2.0 mg LDL-cholesterol/ml) isolated from venous blood of healthy male volunteers stimulated dose-dependently the malondialdehyde (MDA) formation by frozen human platelets, used as a marker for the activity of the thromboxane synthetase. HDL (0.25 - 1.0 mg HDL-cholesterol/ml) and human serum albumin (1 - 10 mg/ml) had no concentration-dependent influence on the MDA formation. If these results can be extended to in vivo they suggested the strong connection between the prostaglandin and lipoprotein hypothesis of pathogenesis of atherosclerosis.