By Suzanne Rostler

NEW YORK (Reuters Health) - The mineral selenium has been shown to lower the risk of certain cancers, but until now, its exact mechanism of action has been unclear.

In a new study, researchers reveal that selenomethionine, a component of selenium, activates a tumor-suppressing gene, p53. This gene prevents tumors from developing by causing abnormal cells to "commit suicide," or preventing them from replicating. The p53 gene is mutated or inactive in many types of cancer.

But the researchers found that selenomethionine appeared to boost p53 activity only in the presence of another compound, Ref1. When researchers eliminated Ref1 from cells, p53 was not activated, according to the report in the Proceedings of the National Academy of Sciences Early Edition.

The results underscore the importance of good nutrition for cancer prevention, Dr. Martin L. Smith, the study's primary author, told Reuters Health. He said that while selenium is found in foods such as nuts, vegetables and enriched grains, most people probably fall short of the recommendation to consume about 50 micrograms (mcg) daily.

"Given the average American diet, multivitamins are probably a good idea for most people," Smith said. According to the study, the recommendation for cancer prevention is about 200 mcg daily.

"Our study is important because it identifies a critical tumor suppressor gene as a...target for selenium," said Smith, from Indiana University in Indianapolis. He added, "a better understanding of the molecular basis for antioxidants' action...will allow a fine-tuning of tumor suppression and cancer prevention."

Antioxidants such as selenium neutralize free radicals in the body. Free radicals are the natural byproducts of normal body processes, but can damage cells and lead to disease.

The findings are based on experiments performed on human lung cancer cells that had no p53 genes. Researchers introduced the gene and treated some of the cells with selenium in the form of selenomethionine.

SOURCE: Proceedings of the National Academy of Sciences Early Edition 2002;10.1073/pnas.212319799.

Last Updated: 2002-09-23 17:00:37 -0400 (Reuters Health)