Printer Friendly

Smoking: clues to its heart effects.

Smoking: Clues to its heart effects

Though it has long been known that cigarette smoking increases one's risk of heart disease, why has remained a mystery. Now scientists at Kyoto University in Japan report some provocative clues. Their research indicates that cigarette-smoke extract can modify low-density lipoproteins (LDLs) -- the so-called "bad" lipoproteins--enhancing their role in the laying down of artery-clogging plaque.

The Japanese study involved LDLs and "scavenger" cells called macrophages isolated from animals and incubated outside the body. However, writing in the April PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES (Vol.85, No.7), Masayuki Yokode and colleagues conclude that if similar LDL modification occurs in humans, it "could explain the increased incidence of atherosclerosis and coronary heart disease in smokers."

The researchers extracted LDLs from the blood of rabbits and exposed the LDLs to the smoke extract, then incubated them in a petri dish with macrophages collected from mice. Similar macrophages can be found along the inside surfaces of human arteries. When blood contains too much LDL or cholesterol for the liver to filter out, these arterial macrophages interact with LDLs and "unload their cholesterol," initiating a process that culminates in the laying down of atherosclerotic plaque, according to Elliott Berlin at the Agriculture Department's Lipid nutrition Laboratory in Beltsville, MD.

The Japanese researchers report that, compared with untreated LDLs, their smoke-treated lipoproteins not only were gobbled up more readily by the macrophages, but also stimulated the conversion of 12.5 times more LDL-cholesterol into cholesteryl ester. (This ester, Berlin points out, is the chemical form in which cholesterol is deposited in the arteries.) The Japanese researchers ended up with macrophages filled with lipids.

Atherosclerosis begins with an accumulation along artery walls of "foam" cells rich in lipids -- mostly cholesteryl esters, explains Daniel Steinberg, an endocrinologist from the Universtiy of California at San Diego. Though normal LDLs won't convert macrophages into foam cells, modified LDLs can sometimes initiate this conversion. "Our work has shown that if you oxidize LDLs...you can get foam cell formation [from macrophages]," Steinberg says. But what makes the Japanese findings so "intriguing," Steinberg adds, is that the cigarette-smoke extract's potent modification of LDLs was not due to oxidation. "That's very interesting," Steinberg says, "and should be pursued."
COPYRIGHT 1988 Science Service, Inc.
No portion of this article can be reproduced without the express written permission from the copyright holder.
Copyright 1988, Gale Group. All rights reserved. Gale Group is a Thomson Corporation Company.

Article Details
Printer friendly Cite/link Email Feedback
Author:Raloff, Janet
Publication:Science News
Date:Apr 30, 1988
Words:374
Previous Article:Circum-inde-cision.
Next Article:Epileptic PET probes: brain imaging is coming of age in the evaluation of infants and children with uncontrolled seizures.
Topics:


Related Articles
More nails in smoking's coffin.
Nicotine: a drug of choice?
Smoking, heart attack link.
Smoking raises female heart attack risk.
Lungs hit harder by pot than by cigarettes.
Older smokers still helped by quitting.
Pictures show smoking's ill effects on DNA.
Heart risk drops in women ex-smokers.
More evidence ties smoke to artery disease.
The plaque of the matter.

Terms of use | Copyright © 2016 Farlex, Inc. | Feedback | For webmasters