Pulling antioxidants starves cancers
By Janet Raloff
Ads on television and in health-food stores extol the benefits of antioxidant vitamins, but they don’t mention that cancerous tissues may depend even more than healthy ones on access to antioxidants. In fact, scientists have just devised an anti-antioxidant dietary therapy that suppresses breast cancer in rodents.
Previously, Craig D. Albright’s team at the University of North Carolina in Chapel Hill had shown that some tumors turn off a normal process that leads to cell suicide, or apoptosis. This path to apoptosis can be promoted by reactive oxygen-bearing molecules, such as hydrogen peroxide and hydroxyl radicals, which antioxidants ordinarily keep in check.
Because cancerous tissues tend to produce excesses of these same reactive molecules, Albright’s group tried removing vitamins A and E–both antioxidants–from the diet of mice bred to spontaneously develop brain cancer. At once, cells in the animals’ tumors exhibited high rates of apoptosis and tumor growth slowed. That was about a year ago.
Now, Albright reports testing the same dietary strategy in mice genetically engineered to develop a lethal cancer that biologically resembles human breast malignancies.
When 80 animals were 9 weeks old and still free of palpable cancer, the researchers switched half of them to chow lacking vitamins A and E. Six weeks later, all mice had one or two breast tumors. However, tumors in rodents that had eaten the vitamin-depleted diet were only half as big and had spawned only one-quarter as many secondary tumors in the lungs. The tumors in these animals also had elevated concentrations of reactive oxygen molecules and several times as much oxidative damage to their DNA and other vital cellular constituents.
Excess apoptosis appears to have contributed to the lower cancer growth in antioxidant-starved animals. Compared with tumors in the other mice, the antioxidant-deprived rodents had apoptosis rates three times as high in their primary tumors and twice as high in their lung tumors.
The new data indicate that some benefits of the antioxidant depletion may trace to its boosting of a gene, NM23H1, that normally suppresses cancer’s spread. Other scientists had found the gene’s activity is low in human breast cancers that have spawned tumors elsewhere. Albright notes that in cancers from the vitamin-depleted mice, the gene’s activity was clearly elevated. Until now, no one realized this gene might be susceptible to dietary manipulation, he told Science News.
Because all plant-based foods contain vitamin E, Albright cautions anyone against trying to rid his or her diet of this antioxidant. He suspects that a better strategy would be to alter the balance of specific antioxidants in the diet. For instance, vitamin C regenerates vitamin E after the latter has sopped up reactive oxygen species. By limiting vitamin C, he says, “we might induce oxidative stress” that kills tumor cells.