January 3, 2003 WASHINGTON (AP) -- Nicotine makes smoking addictive and is bad for the heart, but 60 other cigarette chemicals are blamed for causing cancer. Now some biochemists say nicotine might help set the stage for those chemicals to do their dirty work.
Certain tobacco chemicals trigger cellular genetic damage. Damaged cells are supposed to commit suicide; if they do not, the damage eventually accumulates enough to turn cancerous.
Nicotine activates an enzyme reaction that inhibits cellular suicide, says new research by scientists at the National Cancer Institute.
Nicotine starts activating that enzyme, called Akt, within minutes, while cancer-causing genetic damage takes hours to begin, NCI researchers report in Thursday's Journal of Clinical Investigation. That suggests nicotine -- along with other chemicals that also block cell suicide -- may make cells more vulnerable to the cancer-causers.
"Nicotine is not a carcinogen and we're not trying to make that argument," said the study leader, Dr. Phillip Dennis. But "it may have a permissive effect" for cancer formation.
Scientists first discovered nicotine may block cell suicide 10 years ago, said nicotine expert Dr. Neal Benowitz of the University of California, San Francisco. But the new research uncovers the actual enzyme involved.
That enzyme pathway could prove important in developing cancer-preventing drugs, Dennis said. The immediate question is whether the effect matters for people using nicotine in gum or patches in an effort to kick the habit.
"It's clearly better for people to stop smoking and use a patch than to continue smoking," Dennis said. But the study reinforces that anti-smoking medicines are for short-term use because "there may be biologic consequences" of using patches for months or years, he added.
But Benowitz said the NCI study used cells in laboratory dishes, while previous studies of snuff users -- who do not absorb nearly as many carcinogens as smokers -- suggest there is little cancer risk from nicotine.
Copyright 2003 The Associated Press. All rights reserved.
