Abstract
Because of the ever-increasing incidence of ultraviolet light B (UVB)-induced skin cancer, considerable attention is being paid to prevention through the use of both sunscreens and after sun treatments, many of which contain antioxidants. Vitamin E is included as an antioxidant in many sunscreens and lotions currently on the market. Studies examining the efficacy of vitamin E as a topical preventative agent for UVB-induced skin cancer have yielded conflicting results. A likely contributor to differences in study outcome is the stability of vitamin E in the particular formulation being tested. In the current study we examined the effects of topical vitamin E alone as well as vitamin E combined with vitamin C and ferulic acid in a more stable topical formula (C E Ferulic®). Mice were exposed to UVB for 10 weeks in order to induce skin damage. Then, before the appearance of any cutaneous lesions, mice were treated for 15 weeks with a topical antioxidant, without any further UVB exposure. We found that topical C E Ferulic decreased tumor number and tumor burden and prevented the development of malignant skin tumors in female mice with chronically UVB-damaged skin. In contrast, female mice chronically exposed to UVB and treated topically with vitamin E alone showed a trend towards increased tumor growth rate and exhibited increased levels of overall DNA damage, cutaneous proliferation, and angiogenesis compared to vehicle-treated mice. Thus, we have demonstrated that topical 5% alpha tocopherol may actually promote carcinogenesis when applied on chronically UVB-damaged skin while treating with a more stable antioxidant compound may offer therapeutic benefits.
Highlights
Over two million people are diagnosed with a form of nonmelanoma skin cancer (NMSC) each year in the United States, making skin cancer more prevalent than all other cancers combined [1]
Mice that were exposed to ultraviolet light B (UVB) but received no vehicle treatment did not exhibit a significantly different tumor burden compared to mice treated with vehicle, indicating that the vehicle had no significant effect on tumorigenesis in this study
Because the skin is constantly exposed to external stimuli, it has developed a system of endogenous antioxidants to deal with environmental challenges
Summary
Over two million people are diagnosed with a form of nonmelanoma skin cancer (NMSC) each year in the United States, making skin cancer more prevalent than all other cancers combined [1]. Squamous cell carcinoma (SCC), a malignant form of NMSC, makes up about 16% of all skin cancers. With the increasing NMSC incidence, there has been a renewed focus on sunscreens and other methods of preventing skin cancer, including antioxidant supplementation in food, sunscreens, and lotions. Endogenous antioxidants play an important role in detoxifying ROS and maintaining cutaneous homeostasis. If ROS levels overwhelm the cutaneous antioxidant networks, the cells will be subjected to oxidative stress [2]. Major mechanisms by which ROS foster skin tumor development include induction of DNA damage [3,4], inflammation [5], and angiogenesis [6,7,8]
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