Thursday, March 31, 2011

Smoking Damages DNA Within Minutes

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A stark warning to those tempted to start smoking.

Cigarettes start to destroy a smoker's DNA within minutes of inhaling, new research indicates, suggesting that the habit causes immediate genetic damage and quickly raises the short-term risk for cancer.

The report, the first human study to detail the way certain substances in tobacco cause DNA damage linked to cancer, appears in Chemical Research in Toxicology, one of 38 peer-reviewed scientific journals published by the American Chemical Society.

Globally, lung cancer claims a toll of 3,000 lives each day, largely as a result of cigarette smoking. Smoking also is linked to at least 18 other types of cancer. Evidence indicates that harmful substances in tobacco smoke termed polycyclic aromatic hydrocarbons, or PAHs, are one of the culprits in causing lung cancer.

PAHs are known to inflict damage on DNA. To date, however, little had been known about the exact mechanism by which PAH exposure causes disease.

To better understand the risks, Stephen S. Hecht, Ph.D., and collegues added a labeled PAH, phenanthrene, to cigarettes and tracked its fate in 12 volunteers who smoked the cigarettes. They found that phenanthrene quickly forms a toxic substance in the blood known to cause havoc on the DNA, causing mutations that can cause cancer.

The smokers developed maximum levels of the substance in a time frame that surprised even the researchers: Just 15-30 minutes after the volunteers finished smoking. Researchers said the speed with which the potentially lethal DNA assault began was comparable to having injected the PAH directly into an individual's bloodstream.

Journal Reference:

Yan Zhong, Steven G. Carmella, Pramod Upadhyaya, J. Bradley Hochalter, Diane Rauch, Andrew Oliver, Joni Jensen, Dorothy Hatsukami, Jing Wang, Cheryl Zimmerman, and Stephen S. Hecht. Immediate Consequences of Cigarette Smoking: Rapid Formation of Polycyclic Aromatic Hydrocarbon Diol Epoxides. Chem. Res. Toxicol., 2011, 24 (2), pp 246–252. DOI: 10.1021/tx100345x

Not convinced? Read the full text article HERE

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