he conventional wisdom of how antioxidants such as vitamin C help prevent cancer growth is that they grab up volatile oxygen free radical molecules and prevent the damage they are known to do to our delicate DNA. The Hopkins study, led by Chi Dang, M.D., Ph.D., professor of medicine and oncology and Johns Hopkins Family Professor in Oncology Research, unexpectedly found that the antioxidants' actual role may be to destabilize a tumor's ability to grow under oxygen-starved conditions. Their work is detailed this week in Cancer Cell.
"The potential anticancer benefits of antioxidants have been the driving force for many clinical and preclinical studies," says Dang. "By uncovering the mechanism behind antioxidants, we are now better suited to maximize their therapeutic use."
"Once again, this work demonstrates the irreplaceable value of letting researchers follow their scientific noses wherever it leads them," Dang adds.
The authors do caution that while vitamin C is still essential for good health, this study is preliminary and people should not rush out and buy bulk supplies of antioxidants as a means of cancer prevention.
The Johns Hopkins investigators discovered the surprise antioxidant mechanism while looking at mice implanted with either human lymphoma (a blood cancer) or human liver cancer cells. Both of these cancers produce high levels of free radicals that can be suppressed by feeding the mice supplements of antioxidants, either vitamin C or N-acetylcysteine (NAC).
However, when the Hopkins team examined cancer cells from cancer-implanted mice not fed the antioxidants, they noticed the absence of any significant DNA damage. "Clearly, if DNA damage was not in play as a cause of the cancer, then whatever the antioxidants were doing to help was also not related to DNA damage," says Ping Gao, Ph.D, lead author of the paper.
That conclusion led Gao and Dang to suspect that some other mechanism was involved, such as a protein known to be dependent on free...