Wednesday October 1 2008
Vitamin C was seen to interact with anti-cancer drugs in the laboratory
“Vitamin C supplements could cut the effectiveness of cancer drugs”, reports the Daily Mail. US scientists have found that, in the laboratory, cancer cells treated with vitamin C resist drug treatment by up to 70% and “tumours grew more rapidly”, the newspaper says.
This study used laboratory and animal models of leukaemia and lymphoma, and found that vitamin C decreased the cancer-killing properties of a number of common anti-cancer drugs. However, the study used cells in the laboratory, which limits the application of the results to humans.
If people who are taking anti-cancer drugs are concerned, they could avoid taking additional vitamin C supplementation. However, readers should not be concerned about normal daily intake of vitamin C through a balanced diet, as it remains an important nutrient for human health.
Where did the story come from?
Mark Heaney and colleagues at Memorial Sloan-Kettering Cancer Center and Herbert Irving Comprehensive Cancer Center, New York Presbyterian Hospital, Columbia University, New York, carried out this research. The study was funded by the New York State Department of Health, and with grants from the National Institute of Health, Leukaemia and Lymphoma Society, a Doris Duke Distinguished Clinical Science Award and the Lewis Family Foundation. It was published in the peer-reviewed medical journal, Cancer Research.
What kind of scientific study was this?
This was a laboratory study. The researchers were interested in finding out if vitamin C – an antioxidant – would block the effects of anti-cancer drugs that are known to generate reactive oxygen species as part of their mode of action. This study aimed to investigate this in the laboratory using leukaemia and lymphoma cells and commonly used cancer drugs, including doxorubicin, cisplatin, vincristine, methotrexate and imatinab. The researchers investigated the effect of the drugs on the cells when they had been treated with the chemical form of vitamin C used in the body (dehydroascorbic acid), and when there had been no treatment.
The researchers looked at the effects of pre-treatment with dehydroascorbic acid on cancer cell viability, cell death, the clone-generating properties of the cells, reactive oxygen species and effects upon the mitochondria within the cells (the structures that provide the chemical energy source of the cell). The cytotoxic (cell-killing) properties of the cancer drugs were investigated by looking at the formation of new colonies of cancer cells.
The researchers used cultures of human chronic myeloid leukaemia and lymphoma cells, as well as creating a ‘mouse model’ by injecting mice with lymphoma cells. The human cells were incubated in the laboratory with an ascorbic acid solution. Ascorbic acid had been incubated with ascorbate oxidase to generate dehydroascorbic acid (vitamin C). Following incubation with the vitamin C substances, the cells were incubated for two days with the anti-cancer drugs and then assessed. The mice that had developed palpable tumours after the lymphoma injections were injected with vitamin C and doxorubicin or doxorubicin alone before being killed humanely. The dimensions of the tumours and drug levels were then assessed.
What were the results of the study?
Treatment with dehydroascorbic acid caused a decrease in the cell-killing (cytotoxic) properties of the anti-cancer drugs, with a dose-dependent effect (higher dehydroascorbic acid doses had greater effect). In the mouse model, when vitamin C was administered before treatment with doxorubicin significantly larger tumours were seen than among the mice that had been treated with doxorubicin only.
The decrease in the cell-killing properties of the drugs did not appear to be due to the effects of vitamin C upon the reactive oxygen species in the cells, suggesting that this was not the method of the cell protection. However, vitamin C did appear to prevent the effects that the anti-cancer drugs would normally have upon the electrical potential of the surface membrane of the mitochondria within the cells.
What interpretations did the researchers draw from these results?
The researchers conclude that in this model (which is representative of leukaemia and lymphomas in humans), vitamin C administered before a number of commonly used anti-cancer drugs antagonises the efficacy of the drugs by preserving the electrical potential of the mitochondrial surface membrane. They say that this supports the hypothesis that vitamin C supplementation during cancer treatment may have a detrimental effect upon the efficacy of treatment given.
What does the NHS Knowledge Service make of this study?
This study used models of leukaemia and lymphoma, and examined the effects of a number of common chemotherapy and anti-cancer drugs (which had various mechanisms of actions) when they were administered after treatment with vitamin C. The study found that vitamin C decreased the cancer-killing properties of the drugs by inhibiting the effects that the drugs would normally have upon the mitochondria in the cells.
This study involved applying vitamin C to cancer cells, both human and mouse, in the laboratory. This means its application to live humans is limited. It is unclear how the concentrations of vitamin C (in its various chemical forms) used in the laboratory can be related to those that are achieved by taking vitamin supplements. Vitamin C was applied directly to tumour cells, and this may not be representative of absorption through the body. Also, vitamin C was given two hours before treatment, so it is not possible to tell what the effects would be if the time before treatment was increased or if the vitamin C was given after the drugs.
Nevertheless, these findings will need further research. For now, if people who are taking these anti-cancer drugs are concerned, they could avoid taking additional vitamin C supplementation. Readers should not be concerned about normal daily intake of vitamin C through a balanced diet, as it remains an important nutrient for human health.