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Cigarette smoke is the most common toxin to cause disease and one of the
leading causes of heart disease. Understanding just how cigarette smoke
damages the heart, and particularly DNA in cells in and around the heart,
has been the focus of much research.
One experimental method
of finding where cigarettes smoke is causing harm, and specifically where
it is producing harmful DNA adducts (large, disruptive molecules that
muck up DNA), is to add a radioactive "tracer" to smoke and
then do special tests on the "smoker" to find where the radioactivity
collects. In rats, smoke goes first to the lungs and heart, with a lesser
amount gathering in the liver. After several weeks of exposure to smoke,
the level of DNA adducts in the rats' hearts is twice as high as the level
in their lungs, and several times higher than the levels in their windpipes,
throats, livers or bladders.22
Autopsy studies on
human smokers confirm that the DNA adducts in the heart are higher than
in the lungs.23,24
In addition to pushing
DNA adducts into heart cells, cigarettes smoke also increases oxidative
damage to the DNA and other components of heart cells. Cells in the heart
possess many natural defenses against the damage caused in the process
of converting oxygen to energy, but they lack one of these detoxifying
defenses, namely cytochrome P450. This may explain why heart cells are
particularly vulnerable to the DNA damage of cigarette smoke.25,26
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Animal studies have shown that the level of DNA adducts in the arteries
of rats exposed to cigarette smoke is only slightly lower than the levels
in their hearts and lungs.27 A few autopsies in humans have shown
similar results.28 A larger study was established in the late
1990s in Genoa, Italy, to sample large numbers of human arteries from autopsies
and determine, among other findings, the effects of tobacco smoke on those
arteries.29 Results show that cells from smokers' arteries collect
DNA adducts. The number of DNA adducts found is highest in patients who
had high blood pressure, high cholesterol or advanced age. These DNA adducts,
therefore, are assumed to contribute to the hardening of the arteries or
atherosclerosis that leads to coronary artery disease.30
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As noted by several researchers, the brain has a relatively limited ability
to repair DNA damage that results from oxidative stress and certain toxins.31
Patients with hereditary Alzheimer's disease, both early and late-onset,
have a known defect in the gene for a substance known as amyloid beta protein
precursor. These patients have also been noted to have a lesser capacity
for DNA repair.32
Excessive oxidative stress in the mitochondria, the cells' energy powerhouses,
damages the DNA of those mitochondria, and this too has been linked to
the neurodegenerative diseases of aging.33
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