Potential interaction between antioxidants and cancer treatment

Potential Interaction between Antioxidants and Cancer Treatment

By John Russo Jr./Vicus.com

VICUS.COM (30 April 2000) — Jason Edwards got the surprise of his life on his 50th birthday. The results from his first physical examination in 11 years showed that his cholesterol was slightly elevated. He was overweight, and, oh yes, his prostate specific antigen (PSA) is 8.9 ng/mL (levels greater than 4 ng/mL are considered abnormal). For the first time in his life, Jason, who was a devotee of fast food, had to come to terms with the cumulative effects of past dietary choices on his prostate cancer.

Now, five months following diagnosis and one day after brachytherapy, he is advised by his brachytherapist to stop taking vitamin C each day. There is the possibility that the effects of this antioxidant may counter some of the effects of the 102 radioactive iodine seeds that were placed the day before. Therefore, until the radiation has worn off in about six months, Jason will place his vitamin C therapy on hold.

How might an antioxidant adversely affect brachytherapy?

The precise role that the antioxidant, vitamin C, plays in tumors is not known, but recent studies have shown possible interactions between dietary antioxidants and cancer treatment.

We know that vitamin C is a powerful antioxidant. It consumes free radicals, the toxic substances in the body that can be generated by chemotherapy agents to destroy cancer cells. “It ís possible,” according to Dr. David Golde, Physician-in-Chief at Memorial Sloan-Kettering Cancer Center, “that taking large amounts of vitamin C could interfere with the effects of chemotherapy or even radiation therapy.” These therapies often kill cells, in part, by using oxidative mechanisms. it’s conceivable then, that vitamin C might make cancer treatment less effective, and it is reasonable that cancer patients undergoing chemotherapy avoid taking large amounts of this vitamin.”

Building on past research

Earlier research by Dr. Golde and his colleagues established that specific glucose transporter molecules carry vitamin C into cells. This occurs once vitamin C, which is used by cells in the form of ascorbic acid, is converted into dehydroascorbic acid and transported into the cell. Once inside, the vitamin is converted back to ascorbic acid.

Applying this information to patient care

According to David Agus, an oncologist at Memorial Sloan-Kettering Cancer Center, we now know that tumors acquire and retain large amounts of vitamin C. And their nutritional needs appear to be similar to healthy cells that take in large amounts of the vitamin.”

However, what cancer cells do with the vitamin C after it is absorbed is not known. This will have to be determined before guidelines for the complementary use of antioxidants during chemotherapy and radiation become established.

Furthermore, research from University of T¸bingen, School of Medicine in Germany suggests caution in applying this knowledge to all antioxidants in all types of malignancies. Examination of the modulation of drug-induced cytotoxicity and clonogenic cell death of glioma cells by three structurally unrelated antioxidants (N-acetylcysteine, superoxide dismutase or phenyl-N-tert-butyl-alpha-phenylnitrone) revealed that these antioxidants inhibit acute cytotoxicity and clonogenic cell death induced by cisplatin. However, they had little effect on the toxicity of other cancer drugs including BCNU, doxorubicin, vincristine, cytarabine, or camptothecin.

John Russo, Jr., PharmD, is senior vice president of medical communications at Vicus.com. He is a pharmacist and medical writer with more than 20 years of experience in medical education.


Cancer tumors shown to consume large amounts of vitamin C. Researchers are cautious about cancer patients taking vitamin C supplements. Memorial Sloan-Kettering Cancer Center, 1999. http://www.mskcc.org/tji.htm.

Roller A, Weller M. Antioxidants specifically inhibit cisplatin cytotoxicity of human malignant glioma cells. Anticancer Res, 1998; 18(6A):4493-7.