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Vitamin C enhances DNA damage and cell death in melanoma cells
Last reviewed: 02.07.2025
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A recent study suggests that using ascorbate (vitamin C) to increase DNA damage in melanoma cells may be a more effective way to treat the disease, according to study co-author Marcus Cook, professor and chair of the department of molecular biosciences at the University of South Florida.
The results are published in the journal Free Radical Biology and Medicine.
An interdisciplinary team of researchers found that melanoma cells had more DNA damage and less antioxidant protection than normal skin cells. When treated with hydrogen peroxide and vitamin C, melanoma cells showed even more DNA damage and higher levels of cell death, while normal cells were protected. Additionally, the study results showed that vitamin C enhanced the effectiveness of an existing melanoma drug, eleclomol.
Cook, who also leads the oxidative stress research group, noted that there is a long history of studying the effects of vitamin C on DNA and skin cells, which helped guide them to the current study.
"We have been studying the effects of antioxidants since the late 1990s and were fascinated by vitamin C's ability to act as a prooxidant (causing DNA damage) and antioxidant (preventing DNA damage), as well as its apparent ability to modulate DNA repair. This, combined with our long-standing interest in skin biology/solar UV radiation, also dating back to the 1990s, led us to the present study," Cook said.
"The results show that melanoma cells have higher levels of DNA damage compared to keratinocytes (the main type of cell found in the epidermis). We found that this damage is proportional to the amount of melanin in the melanocytes - the more melanin, the more damage," he explained. "This occurs in cells that have not been exposed to sunlight, indicating that melanin inside the cells can cause damage in melanoma cells."
"Our study shows that levels of potentially harmful reactive species were proportional to the amount of melanin, while levels of protective antioxidants were inversely proportional. Given this, we found that we could exploit this situation to selectively kill melanoma cells," he added.
Cook acknowledges that additional clinical research and trials will strengthen these findings and help move toward incorporating ascorbate into treatment.
"Given that ascorbate has already been well studied and is known to be well tolerated, I believe that clinicians could incorporate ascorbate into existing treatments to augment existing approaches if they act by inducing DNA damage, as elesclomol does," he said. "The oxidative stress biomarkers we use in my lab's Oxidative Stress Research Group are particularly suitable for clinical trials, and we could support in vivo biomonitoring of patients if clinical trials begin."