Excessive, long-term sun exposure is one of the causes of so-called "white skin cancer". Excessive exposure to UV rays can damage the DNA in the cell nucleus to such an extent that the natural "repair mechanism" is no longer able to cope. This results in the formation of cyclobutane pyrimidine dimers (CPD). In turn, these cause skin cancer due to the continual process of cell multiplication by cell division and can block the immune response. However, recent research increasingly suggests that sunshine itself can prevent and even cure "white skin cancer".
Laboratory experiments on mice carried out by researchers at the University of Sydney in Australia have shown how vitamin D in its active form (1,25(OH)2D3) can inhibit the multiplication of abnormal cells. The researchers discovered that this dangerous process can be slowed down or even halted by active vitamin D. In their laboratory tests, this resulted in much rarer occurrences of white skin cancers such as spinalioma (squamous-cell carcinoma) and benign epithelial tumours (papilloma).
The active form of vitamin D is 90% produced by a complicated metabolic process triggered by UV radiation from sunlight on the skin. This process involves the liver, the kidneys and the skin cells themselves. "Generally, just a few minutes in the sun are enough to trigger this process - long before the UV rays have begun to cause irreparable damage to the DNA of the skin cells. So it's a question of getting just the right amount of sunshine in order to benefit from the positive effects of UV exposure, while avoiding the negative consequences", Ad Brand of the Sunlight Research Forum explains.
Source:
Katie M. Dixon, Anthony W. Norman, Vanessa B. Sequeira, Ritu Mohan, Mark S. Rybchyn, Vivienne E. Reeve, Gary M. Halliday, and Rebecca S. Mason: "1a,25(OH)2-Vitamin D and a Nongenomic Vitamin D Analogue Inhibit Ultraviolet Radiation-Induced Skin Carcinogenesis"; in: Cancer Prevention Research, 4(9) September 2011
Laboratory experiments on mice carried out by researchers at the University of Sydney in Australia have shown how vitamin D in its active form (1,25(OH)2D3) can inhibit the multiplication of abnormal cells. The researchers discovered that this dangerous process can be slowed down or even halted by active vitamin D. In their laboratory tests, this resulted in much rarer occurrences of white skin cancers such as spinalioma (squamous-cell carcinoma) and benign epithelial tumours (papilloma).
The active form of vitamin D is 90% produced by a complicated metabolic process triggered by UV radiation from sunlight on the skin. This process involves the liver, the kidneys and the skin cells themselves. "Generally, just a few minutes in the sun are enough to trigger this process - long before the UV rays have begun to cause irreparable damage to the DNA of the skin cells. So it's a question of getting just the right amount of sunshine in order to benefit from the positive effects of UV exposure, while avoiding the negative consequences", Ad Brand of the Sunlight Research Forum explains.
Source:
Katie M. Dixon, Anthony W. Norman, Vanessa B. Sequeira, Ritu Mohan, Mark S. Rybchyn, Vivienne E. Reeve, Gary M. Halliday, and Rebecca S. Mason: "1a,25(OH)2-Vitamin D and a Nongenomic Vitamin D Analogue Inhibit Ultraviolet Radiation-Induced Skin Carcinogenesis"; in: Cancer Prevention Research, 4(9) September 2011
