Interaction of Ascorbic Acid and Tocopherolon β-Carotene Modulated Carcinogenesis

Abstract

Epidemiological studies suggested that above average intake of β-carotene (βC) might reduce cancer risks. However, clinical trials found that βC supplementation did not reduce the occurrence of non-melanoma skin cancer and that smokers suffered a significant increase in lung cancer incidence. Further, supplementing semi-defined diets with βC failed to provide photoprotection as reported earlier for closed-formula rations, but actually exacerbated carcinogenesis. A redox mechanism, based upon one-electron transfer rate constants, proposed interactions between tocopherol, βC and ascorbic acid in which the carotenoid radical cation, a strongly oxidizing radical, would be repaired by ascorbic acid. If the carotenoid radical cation remained unrepaired, this strongly oxidizing species could account for the pro-carcinogenic activity of βC. Data from nutritional studies supported an interaction of tocopherol and βC but not with ascorbic acid. The repair of the βC radical cation must be dependent on factors other than ascorbic acid, e.g., other carotenoids or unidentified phytochemical(s).

Keywords:

• Antioxidants
• Cancer
• Free radicals
• Ascorbic acid
• Tocopherol
• β-Carotene (βC)