Abstract
Skin cells are constantly exposed to reactive oxygen species (ROS) and oxidative stress from exogenous and endogenous sources. UV radiation is the most important environmental factor in the development of skin cancer and skin aging. The primary products caused by UV exposure are generally direct DNA oxidation or generation of free radicals which form and decompose extremely quickly but can produce effects that can last for hours, days, or even years. UV-induced generation of ROS in the skin develops oxidative stress when their formation exceeds the antioxidant defense ability. The reduction of oxidative stress can be achieved on two levels: by lowering exposure to UVR and/or by increasing levels of antioxidant defense in order to scavenge ROS. The only endogenous protection of our skin is melanin and enzymatic antioxidants. Melanin, the pigment deposited by melanocytes, is the first line of defense against DNA damage at the surface of the skin, but it cannot totally prevent skin damage. A second category of defense is repair processes, which remove the damaged biomolecules before they can accumulate and before their presence results in altered cell metabolism. Additional UV protection includes avoidance of sun exposure, usage of sunscreens, protective clothes, and antioxidant supplements.
Highlights
Ultraviolet radiation (UVR) is an essential risk factor for the development of premalignant skin lesions as well as of melanoma and nonmelanoma skin cancer
Many other studies confirmed that acute exposure of human skin to UVR in vivo leads to oxidation of cellular biomolecules that could be prevented by prior antioxidant treatment
Skin DNA molecules are constantly “bombarded” by reactive oxygen species (ROS) originating from endogenous processes as well as from environmental agents and from radiation sources
Summary
Ultraviolet radiation (UVR) is an essential risk factor for the development of premalignant skin lesions as well as of melanoma and nonmelanoma skin cancer. DNA damage due to reactive oxygen species formation is not a rare event since it is estimated that human cell sustains an average of 105 oxidative hits per day due to cellular oxidative metabolism [4], DNA is functionally very stable, so that the incidence of cancer is much lower than one would expect, taking into account the high frequency of oxidative hits It seems that in rapidly dividing epithelium, such as the epidermis, nuclear damage triggered by some xenobiotics may not be so important because of the constant introduction of new healthy cells, whereas a DNA mutation has a much higher probability to become fixed to a transformed phenotype in tissues (e.g., liver) with slow cell turnover [5]. There still remains the answer regarding controversial data on the use of synthetic antioxidants in cancer prevention and treatment
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