Cigarette smoke-induced depression in LCAT activity

Abstract

The effect of acute inhalation of cigarette smoke on plasma cholesterol esterification by lecithin-cholesterol acyltransferase (LCAT) in atherosclerosis-susceptible White Carneau pigeons was examined. Pigeons were assigned to four treatment groups: (1) Shelf Control fed a chow diet and not exposed to smoke products; (2) Sham pigeons fed a cholesterol-saturated fat diet and exposed to fresh air by the Lorillard smoking machine; (3) low nicotine-low carbon monoxide (LoLo) animals also fed the cholesterol diet and exposed to low concentrations of these cigarette smoke products; and (4) high nicotine-high carbon monoxide (HiHi) birds fed the cholesterol diet and subjected to high concentrations of these inhalants. Both Control and Sham birds had significantly higher LCAT activity (percentage esterification per minute) than HiHi pigeons. Experiments designed to determine whether altered enzyme and/or substrate were responsible for depressed activity revealed no smoke-related modification in substrate efficiency. In addition, Sham and HiHi pigeons had similar concentrations of plasma-free cholesterol, high density lipoprotein (HDL) cholesterol, cholesteryl ester and phospholipid, and similar HDL phospholipid and cholesteryl ester fatty acid profiles. However, reduced LCAT activity in HiHi pigeons can be explained by (1) impairment of enzyme efficiency as estimated by in vitro analysis; and (2) in vivo reduction in levels of LCAT cofactor, HDL apoprotein A-I.