High-dose IV vitamin C selectively kills cancer cells

Treatment with vitamin C or ascorbate at high levels, which can be attained if administered intravenously, can selectively destroy cancer cells, new research indicates.

The destructive effect is mediated by hydrogen peroxide formation at the target tissues. Given the role of endogenous hydrogen peroxide in antimicrobial defense, the researchers believe the current findings could have implications for the treatment of infections as well as cancer. Studies in the 1970s first suggested a role for vitamin C as an anticancer agent, but subsequent studies failed to show a beneficial effect. As it turned out, the earlier studies used a combination of IV and oral delivery, whereas the later studies relied solely on the oral delivery. At the time, it was not fully appreciated that the route of ascorbate delivery might markedly influence plasma levels.Recent research, however, has shown that the much higher plasma levels are attained when the same dose of ascorbate is given intravenously rather than orally. This, among other things, led Dr. Mark Levine, from the National Institutes of Health in Bethesda, Maryland, and colleagues to examine the anticancer effects of ascorbate at levels that would be attainable with IV administration.The researchers' findings appear in the Proceedings of the National Academy of Sciences for September 20.At the concentrations tested, ascorbate was able to destroy several different cancer types, while leaving normal cells unscathed. Further analysis showed that the killing effects did not depend on metal chelators, but required hydrogen peroxide formation.Adding ascorbate to target medium led to hydrogen peroxide formation, whereas adding it to blood did not lead to detectable levels of the free radical. This supports the feasibility of intravenous administration in cancer patients, the authors conclude. They note that a phase I trial is currently underway to gauge the safety of IV ascorbate in patients with advanced cancer.(Source: Proc Natl Acad Sci USA 2005;102:13604-13609: Reuters Health: Oncolink: September 2005.)