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Oxidative Stress and Skin Cancer

Oxidative stress occurs when there is an imbalance between free radicals and antioxidants in the body. When functioning properly, free radicals can help fight off pathogens. However, when there are more free radicals in the body than our antioxidants can handle, the free radicals can start doing damage to fatty tissue, DNA, and proteins. Over time, this damage can lead to various diseases, including cancer.

Risk factors for oxidative stress include ozone, chemicals, cigarette smoke, radiation, pollution, alcohol, extreme physical exertion (including over-exercising), and a diet that is high in sugar.


Sun exposure is the most cited source of oxidative stress, contributing harmful reactive oxygen species (ROS). ROS triggers DNA damage and lipid peroxidation, which can lead to abnormal skin cell growth, and eventually, if left unchecked, skin cancer. UV radiation from the sun is also a major risk when it comes to skin cancer.


It is important to understand the basics about UV rays in order to protect one’s skin and reduce the risk of developing skin cancer.

Research has identified two types of UV light that contribute to skin cancer:
  • Ultraviolet A (UVA) has a longer wavelength and is associated with skin aging. It penetrates our tissue to the bone, causing mutations and destroying Vitamin D. Sunscreen does not block this type of ray.

  • Ultraviolet B (UVB) has a shorter wavelength and is associated with skin burning. UVB rays are not as carcinogenic as UVA rays. They penetrate the skin and are responsible for initiating Vitamin D synthesis. Sunscreen is able to block this type of ray
In most cases, UV exposure results in damage to DNA, but this damage can normally be repaired by the cells. Vitamin D is responsible for stimulating DNA repair responses, which are essential for skin protection.

If the damage from UV exposure is too great, some of the changes may stay on as permanent mutations and lead to skin cancer. One option for lowering skin cancer risk is increasing the body’s levels of antioxidants to defend against damage by reactive oxygen species and oxidative stress.
Vitamin D and Sunscreen
Vitamin D is an essential nutrient, one of the fat-soluble vitamins, and is a precursor of a potent steroid hormone that regulates a broad spectrum of physiological processes. In addition to its classical role in bone metabolism and calcium homeostasis, several studies showed that Vitamin D may play a key role in the prevention and treatment of many autoimmune diseases, including cancer. Vitamin D can be photosynthesized in the skin or obtained from one’s diet. It is then converted by the liver to 25-hydroxyvitamin D, its major circulating form. This form is the best indicator of Vitamin D nutritional status. It is also the hormonal form of the nutrient that is important in metabolic processes to maintain healthy bodily functions.

There are many types of cells in the skin that express the vitamin D receptor and convert circulating 25-hydroxyvitamin D to1,25-dihydroxyvitamin D for local use. This metabolite has been shown to exert potent effects on cellular differentiation, cellular proliferation, and immune regulation. It is theorized that by these mechanisms Vitamin D and its analogues are effective treatment options for any skin disease, including skin cancer.
Insufficient vitamin D nutritional status has been associated with different diseases, most notably cancer. There is evidence that supplementation with Vitamin D reduces the overall incidence of cancer.

Using sunscreen blocks the ability of the skin to photosynthesize Vitamin D. However, chronic sunscreen usage significantly decreases the synthesis of Vitamin D by interfering with UVB rays, which initiate Vitamin D synthesis.

Sunscreens were designed to protect the skin from the sun’s damaging rays. However, nearly all sunscreens contain large amounts of chemicals such as oxybenzone, avobenzone, octisalate, octocrylene, homosalate, octinoxate, retinyl palmitate (synthetic VitA). Even after a single use, all of these ingredients will end up in the bloodstream and urine.
The skin is the body’s largest organ, which absorbs anything applied to it. If an ingredient is not natural, it should not be applied, since it will be absorbed and create more disruption than protection in the body on the molecular level.
Studies show that synthetic Vitamin A can spur excess skin growth, known as hyperplasia, and that in sunlight, retinyl palmitate can form small molecules called free radicals, which damage DNA. The same studies showed that the oral ingestion of natural Vitamin A (an antioxidant) products can reduce the risk of squamous cell carcinoma in people at high risk for skin cancer (MOON 1997). In 2011, Scientists from the National Toxicology Program confirmed that both retinyl palmitate and retinoic acid, another form of Vitamin A, speed up development of cancerous lesions and tumors on UV-treated animals (NTP 2011,2012)

Sunscreen use has not improved skin cancer rates, but its use has contributed to the population’s increasing Vitamin D deficiency by blocking UVB rays, which are responsible for synthesizing Vitamin D. Not only can the use of these products make a person deficient in Vitamin D, but it may also bring significant amounts of toxins that can exacerbate cancer cell proliferation anywhere in the body.
In conclusion, avoiding sunburns and excessive time in the sun will help to maintain healthy skin. Everyone needs sunlight to maintain healthy biological processes in the body, but exposure should only take place from sunrise until about 10 am, when UVB and UVA rays are not as strong and damaging to the skin. One should also make sure to alternate 15 minutes in and 15 minutes out of the sun. Using only natural protection will reduce the severity of sunburns and halt skin cancer cell growth. This can come in the form of products derived from propolis, algae, and lichens, which have shown potential photoprotection properties against UV radiation exposure-induced skin damage. Building up the immune system will also generally enable a better response to oxidative stress.
References
  1. Narendhirakannan RT, Hannah MA. Oxidative stress and skin cancer: an overview. Indian J Clin Biochem. 2013 Apr;28(2):110-5. doi: 10.1007/s12291-012-0278-8. Epub 2012 Nov 23. PMID: 24426195; PMCID: PMC3613501.
  2. Bickers DR, Athar M. Oxidative stress in the pathogenesis of skin disease. J Invest Dermatol. 2006 Dec;126(12):2565-75. doi: 10.1038/sj.jid.5700340. PMID: 17108903.
  3. Trouba KJ, Hamadeh HK, Amin RP, Germolec DR. Oxidative stress and its role in skin disease. Antioxid Redox Signal. 2002 Aug;4(4):665-73. doi: 10.1089/15230860260220175. PMID: 12230879.
  4. D'Orazio J, Jarrett S, Amaro-Ortiz A, Scott T. UV radiation and the skin. Int J Mol Sci. 2013 Jun 7;14(6):12222-48. doi: 10.3390/ijms140612222. PMID: 23749111; PMCID: PMC3709783.
  5. Mohania D, Chandel S, Kumar P, Verma V, Digvijay K, Tripathi D, Choudhury K, Mitten SK, Shah D. Ultraviolet Radiations: Skin Defense-Damage Mechanism. Adv Exp Med Biol. 2017;996:71-87. doi: 10.1007/978-3-319-56017-5_7. PMID: 29124692.
  6. “Vitamin D and Cancer Prevention.” National Cancer Institute, www.cancer.gov/about-cancer/causes-prevention/risk/diet/vitamin-d-fact-sheet.
  7. Jeon SM, Shin EA. Exploring vitamin D metabolism and function in cancer. Exp Mol Med. 2018 Apr 16;50(4):1-14. doi: 10.1038/s12276-018-0038-9. PMID: 29657326; PMCID: PMC5938036.
  8. Sunscreens, EWG's 2020 Guide to. “EWG's 2020 Guide to Safer Sunscreens.” EWG, www.ewg.org/sunscreen/report/the-problem-with-vitamin-a/
  9. DiNardo JC, Downs CA. Dermatological and environmental toxicological impact of the sunscreen ingredient oxybenzone/benzophenone-3. J Cosmet Dermatol. 2018 Feb;17(1):15-19. doi: 10.1111/jocd.12449. Epub 2017 Oct 31. PMID: 29086472.
  10. Krause M, Klit A, Blomberg Jensen M, Søeborg T, Frederiksen H, Schlumpf M, Lichtensteiger W, Skakkebaek NE, Drzewiecki KT. Sunscreens: are they beneficial for health? An overview of endocrine disrupting properties of UV-filters. Int J Androl. 2012 Jun;35(3):424-36. doi: 10.1111/j.1365-2605.2012.01280.x. PMID: 22612478.
  11. Saewan N, Jimtaisong A. Natural products as photoprotection. J Cosmet Dermatol. 2015 Mar;14(1):47-63. doi: 10.1111/jocd.12123. Epub 2015 Jan 12. PMID: 25582033.
  12. Wacker M, Holick MF. Sunlight and Vitamin D: A global perspective for health. Dermatoendocrinol. 2013 Jan 1;5(1):51-108. doi: 10.4161/derm.24494. PMID: 24494042; PMCID: PMC3897598.
Additional Research
  1. Rodríguez-Rodríguez E, Aparicio Vizuete A, Sánchez-Rodríguez P, Lorenzo Mora AM, López-Sobaler AM, Ortega RM. Deficiencia en vitamina D de la población española. Importancia del huevo en la mejora nutricional [Vitamin D deficiency in Spanish population. Importance of egg on nutritional improvement]. Nutr Hosp. 2019 Aug 27;36(Spec No3):3-7. Spanish. doi: 10.20960/nh.02798. PMID: 31368328.
  2. Barysch MJ, Hofbauer GF, Dummer R. Vitamin D, ultraviolet exposure, and skin cancer in the elderly. Gerontology. 2010;56(4):410-3. doi: 10.1159/000315119. Epub 2010 May 21. PMID: 20502035.
  3. Coutinho RCS, Santos AFD, Costa JGD, Vanderlei AD. Sun exposure, skin lesions and vitamin D production: evaluation in a population of fishermen. An Bras Dermatol. 2019 Jul 29;94(3):279-286. doi: 10.1590/abd1806-4841.20197201. PMID: 31365655; PMCID: PMC6668935.