August 27, 2002 | 0 comments

Studies Illuminate Caffeine's Connection to Cancer

By Sarah Graham   

 
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Caffeine's best-known role, especially for early morning java drinkers, is as a stimulant. But two reports published online this week by the Proceedings of the National Academy of Sciences illustrate how the molecule may meddle in cell mutations that could lead to cancer. The good news is that topical application of caffeine inhibits the formation of skin tumors in mice. The bad news is that the molecule represses the repair of genetic mutations caused by low levels of radiation.

In the first study, Allan Conney and his colleagues at Rutgers University applied two components of tea, caffeine and epigallocatechin gallate (EGCG), to the skin of hairless mice that had been heavily exposed to ultraviolet B radiation over the course of 20 weeks but had not yet developed skin tumors. Animals that received the applications had significantly fewer skin tumors--both malignant and benign--than those who did not. In addition, both molecules exhibited highly selective behavior, killing only tumor cells and leaving normal areas of the skin unaffected. The scientists say that caffeine's chemical stability as compared to EGCG makes it a better candidate for further study in humans. "For now, if you are a mouse, it would be terrific," Conney says. "In people, we just don't know yet."

The less encouraging results came from the second study, conducted by Theodore Puck of the Eleanor Roosevelt Institute in Denver and his colleagues. They studied hamster cells exposed to alpha radiation (which is implicated in some cases of lung cancer) and gamma radiation. When caffeine was added to the cells after the radiation exposure, the two types caused similar amounts of genetic damage. In the absence of caffeine, however, cells exposed to alpha radiation exhibited fewer mutations. The findings suggest that alpha radiation-induced genetic mutations can be repaired during cellular division, but that caffeine can hinder the body's own mending mechanisms.



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