New study shows vitamin C boosts DNA damage and cell death in melanoma cells

A recent study shows that there may be a more effective way to treat melanoma by using ascorbate (vitamin C) to increase DNA damage in cancer cells, leading to their death, according to co-corresponding author of the study Marcus Cooke, professor and chair in the Department of Molecular Biosciences at the University of South Florida.

The findings are published in the journal Free Radical Biology and Medicine.

The multi-disciplinary research team found that melanoma cells have more DNA damage and fewer antioxidant defenses compared to normal skin cells. When treated with hydrogen peroxide and vitamin C, melanoma cells showed even more DNA damage and higher cell death rates, while normal cells were protected. Additionally, the study results found that vitamin C boosted the effectiveness of an existing melanoma drug, elesclomol.

Cooke, who also leads the Oxidative Stress Group, said that there is a long-standing history of studying the impact vitamin C has on DNA and skin cells, which helped direct the path to their current study.

“We’ve been studying the effects of antioxidants since the late 1990s and have been fascinated by the ability of vitamin C to act as a prooxidant (causing DNA damage) and antioxidant (preventing DNA damage), and its apparent ability to help modulate DNA repair. This, coupled with our long-standing interest in skin biology/solar ultraviolet radiation, also dating back to the 1990s, led us to the present study,” Cooke said.

“The findings show that melanoma cells have higher levels of DNA damage than keratinocytes (the primary type of cell found in the epidermis). We discovered that this damage was proportional to the amount of melanin that is in the melanocytes—the more melanin, the more damage,” he explained. “This is in cells not even exposed to sunlight, suggesting that melanin within cells can cause damage in melanoma cells.”

“Our study reveals that levels of potentially harmful reactive species were proportionate to the amount of melanin, and the levels of protective antioxidants inversely proportional. With all this in mind, we went on to discover that we can exploit this situation to selectively kill melanoma cells,” he added.

Cooke acknowledges that additional clinical studies and trials would bolster these findings and assist in moving towards including ascorbate as an accessory in treatment.

“Given that ascorbate is already well studied and is known to be well tolerated, I think that clinicians could include ascorbate as an addition to existing treatment to enhance existing approaches if they act by inducing DNA damage as elesclomol does,” he said. “The biomarkers of oxidative stress that we use in my Oxidative Stress Group laboratory are particularly suitable for clinical studies, and we could help support in vivo (whole living cell organisms) biomonitoring of patients, should clinical studies get underway.”