Sunlight Vitamin D and Skin Cancer

Abstract

Today, there is a controversial debate in many scientific and public communities on how much sunlight is appropriate to balance between the positive and negative effects of solar UV-exposure. UV exposure undoubtedly causes DNA damage of skin cells and is a major environmental risk factor for all types of skin cancers. In geographic terms, living in parts of the world with increased erythemal UV or high average annual bright sun results in increased risks of skin cancers, with the greatest increased risk for squamous cell carcinoma, followed by basal cell carcinoma and then melanoma. On the other hand, sunlight exerts positive effects on human health, that are mediated in part via UV-B-mediated cutaneous photosynthesis of vitamin D. It has been estimated that at present, approximately 1 billion people worldwide are vitamin D-deficient or -insufficient. This epidemic causes serious health problems that are still widely under-recognized. Vitamin D deficiency leads to well documented problems for bone and muscle function. There are also associations between vitamin D-deficiency and increased incidence of and/or unfavourable outcome for a broad variety of independent diseases, including various types of malignancies (e.g. colon-, skin-, and breast cancer), autoimmune diseases, infectious diseases, and cardiovascular diseases. In this review, the present literature is analyzed to summarize our present knowledge about the important relationship of sunlight, vitamin D and skin cancer.

Observing and Understanding the Ultrafast Photochemistry in Small Molecules: Applications to Sunscreens

“…The human body has a number of mechanisms at its disposal in order to prevent, protect, or repair damage from the adverse effects of UVR over-or underexposure. For example, UVR induced DNA damage can be repaired by nucleotide/base excision or, in the case of severely damaged cells, apoptosis can prevent the replication of a damaged genome 9 . These mechanisms are reserved as a 'last resort' to DNA damage; skin pigmentation is the primary photoprotective mechanism found in humans.…”

Tumor suppression in skin and other tissues via cross-talk between vitamin D- and p53-signaling

“…The epidermis contains a basal layer (stratum basale), that is composed of self-renewing cells (keratinocytes) with limited proliferative capacity (transient amplifying cells), of stem cells with high proliferative capacity that need to be preserved, and of outwardly migrating layers (stratum spinosum, stratum granulosum and stratum corneum) of mostly resting keratinocytes at different stages of differentiation. The skin is one of the key tissues of the human body's vitamin D regulatory network (VDRN) (Lehmann et al, 2004; Holick, 2007; Reichrath and Reichrath, 2012; Mason and Reichrath, 2013). First, vitamin D is synthesized in the skin (Figure 1) by the action of solar or artificial ultraviolet B (UVB) radiation (under most living conditions, only a small amount of vitamin D is taken up by the diet) (Lehmann et al, 2004; Holick, 2007).…”

Photodynamics of potent antioxidants: ferulic and caffeic acids

“…mutagenesis in DNA. 2 This can lead to cancers of the skin, such as malignant melanoma, [3][4][5] of which worldwide incidences are on the increase. 6 While human skin has a natural photoprotective mechanism in the form of tanning, it is a delayed response during which photodamage can occur.…”