Abstract

A study was carried out to examine the effect of chronic nicotine administration on tissue content of, and incorporation of acetate-1-C¹⁴ into, cholesterol, cholesterol ester, glycerides, phospholipids and free fatty acids in liver, serum, heart and brain of the dog. A significant diminution was observed in the rate of cholesterol synthesis in nicotine-treated animals, with the greatest reduction being in the synthesis of serum cholesterol (-68%), followed by liver (-64%), brain (-50%) and heart muscle (-37%) cholesterol. A significant decrease was also observed in the incorporation of acetate-1-C¹⁴ into the cholesterol moiety of cholesterol esters in liver (-57%) and serum (-69%) of nicotine-treated animals. The incorporation of acetate-1-C¹⁴ into fatty acids, free or esterified, remained unaltered in the experimental animals. The tissue content of lipids remained identical in control and nicotine-treated animals, except for a small but statistically significant decrease in cholesterol content of liver (-11%) and heart muscle (-7%). The biologic half-life of exogenous cholesterol-4-C¹⁴ was significantly longer in nicotine-treated animals than in control animals. The relationship between nicotine metabolism, and the selective diminution in acetate-1-C¹⁴ incorporation into cholesterol, and reduced cholesterol turnover of nicotine-treated animals is discussed.