Vitamin C is a powerful antioxidant that can lower a person's risk of developing a number of diseases. But it may also reduce the effectiveness of anti-cancer medication, new research suggests.
Scientists from Memorial Sloan-Kettering Cancer Center treated cancer cells with vitamin C and found that chemotherapy drugs killed between 30 and 70 per cent fewer of them, depending on the drug used.
When the researchers implanted cancer cells treated with vitamin C into mice, they found that those tumours grew more rapidly than tumours that were left untreated by the vitamin.
The findings suggest that "the use of vitamin C supplements could have the potential to reduce the ability of patients to respond to therapy," study author Dr. Mark L. Heaney, an associate attending physician at Memorial Sloan-Kettering, said in a statement.
The research was conducted by scientists at Memorial Sloan-Kettering and Columbia University in New York. The study is published in the journal Cancer Research.
Research into the effect of vitamin C on cancer treatment has so far been mixed. Some studies show that it may benefit cancer patients because it is an antioxidant. This means it can reduce disease risk by warding off the damage to DNA caused by free radicals.
However, some forms of chemotherapy produce free radicals that kill the mitochondria, or the power source, of cancer cells. The researchers found that the vitamin C was protecting the mitochondria of the cancer cells, which kept them alive.
The findings do not mean that cancer patients should reduce the amount of vitamin C they are getting from a healthy diet, Heaney said.
However, it is the larger doses of vitamin C that patients get from supplements that may alter the efficacy of their treatment.
The researchers also caution that the study was conducted on mice. However, they are confident the findings will be replicated in human studies.
Abstract:
Vitamin C Antagonizes the Cytotoxic Effects of Antineoplastic Drugs
Mark L. Heaney, Jeffrey R. Gardner, Nicos Karasavvas, David W. Golde, David A. Scheinberg, Emily A. Smith and Owen A. O'Connor
Vitamin C is an antioxidant vitamin that has been hypothesized to antagonize the effects of reactive oxygen species-generating antineoplastic drugs. The therapeutic efficacy of the widely used antineoplastic drugs doxorubicin, cisplatin, vincristine, methotrexate, and imatinib were compared in leukemia (K562) and lymphoma (RL) cell lines with and without pretreatment with dehydroascorbic acid, the commonly transported form of vitamin C. The effect of vitamin C on viability, clonogenicity, apoptosis, P-glycoprotein, reactive oxygen species (ROS), and mitochondrial membrane potential was determined. Pretreatment with vitamin C caused a dose-dependent attenuation of cytotoxicity, as measured by trypan blue exclusion and colony formation after treatment with all antineoplastic agents tested. Vitamin C given before doxorubicin treatment led to a substantial reduction of therapeutic efficacy in mice with RL cell-derived xenogeneic tumors. Vitamin C treatment led to a dose-dependent decrease in apoptosis in cells treated with the antineoplastic agents that was not due to up-regulation of P-glycoprotein or vitamin C retention modulated by antineoplastics. Vitamin C had only modest effects on intracellular ROS and a more general cytoprotective profile than N-acetylcysteine, suggesting a mechanism of action that is not mediated by ROS. All antineoplastic agents tested caused mitochondrial membrane depolarization that was inhibited by vitamin C. These findings indicate that vitamin C given before mechanistically dissimilar antineoplastic agents antagonizes therapeutic efficacy in a model of human hematopoietic cancers by preserving mitochondrial membrane potential. These results support the hypothesis that vitamin C supplementation during cancer treatment may detrimentally affect therapeutic response.
