Extended exposure to ultraviolet (UV) light has been linked to the hastening of skin decline and the development of skin malignancies. Removing the damaging consequences of UV exposure while achieving increased pigmentation has been a consideration of scientific study. An innovative approach has been studying the potential action of research peptides like Melanotan (MT-2), one of a series of select peptides under study and hypothesized to influence skin pigmentation without the necessity of UV exposure which typically induces such pigmentation.
By activating a biological mechanism regulated by the tumor-suppressor gene p53, ultraviolet (UV) light produces an increase in the skin pigment melanin or tanning. Elevated levels of melanin has been considered to support shielding skin cells from ultraviolet (UV) radiation, which may cause cancer, cell death, and the breakdown of extracellular matrix proteins (such as collagen) in the skin by damaging their DNA.
When UV radiation breaks down DNA in the outer layers of the skin, visible impact of DNA damage may be seen. The DNA damage causes the tumor suppressor protein p53 to stabilize and activate. As a result, proopiomelanocortin (POMC) becomes more active. Alpha-melanocyte stimulating hormone (-MSH), a cleaved derivative of proopiomelanocortin, interacts with the melanocortin 1 receptor (MC1R). This results in increased melanin production and increased number of melanocytes. As a result of these factors working together, melanin production increases, and skin becomes darker by degrees. After that, the melanin soaks up the UV rays, protecting the DNA from further deterioration.
Melanin production following UV radiation exposure only occurs following DNA damage. This suggests DNA damage has already happened, increasing cancer risk before exposure. In order to reap the advantages of melanin protection without first triggering DNA damage, current research is focused on boosting melanin formation without exposure to UV radiation.
A Revolutionary New Method
Melanotan, synthetically developed to act as a pigmenting agent, is now being studied for another reason, its proposed ancillary action of increasing arousal signalling in the brain. This has opened new avenues for research and reignited the scientific community's focus on this and similarly sequenced research peptides.
Afamelanotide (Melanotan) Peptide
Melanotan (also known as Melanotan 1) was developed in the 1980s at the University of Arizona and is a synthetic counterpart of -MSH that has been hypothesized to bind to the MC1R. Experimental studies have examined its potential in managing and preventing sun-related skin conditions such as actinic keratosis, squamous cell carcinoma, and erythropoietic protoporphyria. Researchers have speculated that Melanotan may decrease the amount of amyloid plaques in the brains of research models of Alzheimer's Disease. Some research suggests it may stimulate new brain cell proliferation, which may have cognitive impacts.
MT-2 Melanotan Peptide
MT-2 was developed from MT-1. Research suggests its properties may include enhancing sexual excitement, decreasing hormone signalling that indicates brain patterns of addiction, mitigating the symptoms that contribute to the development of diabetes, and reducing hunger hormone release. Because of its potential within the realm of addiction research, it is of special interest. Researchers have focused on Melanotan 2 because of the impacts in arousal that it has been hypothesized to have, even though it is one of the peptides primarily developed for increase in pigmentation. Particularly among male research models who have not exhibited a response from exposure to other compounds, the peptide is being studied as an alternative to PDE inhibitors.
Scientists interested in further studying these compounds can visit biotechpeptides.com for the highest quality research compounds.
References
[i] J Marshall, "Gene behind tanning comes out of hiding," New Scientist.
[ii] H. Chen, Q. Y. Weng, and D. E. Fisher, "UV signaling pathways within the skin," J. Invest. Dermatol., vol. 134, no. 8, pp. 2080–2085, Aug. 2014, doi: 10.1038/jid.2014.161.
[iii] "The science of sunscreen," Harvard Health, Jul. 01, 2018.
[iv] D. Giuliani et al., "Melanocortins protect against brain damage and counteract cognitive decline in a transgenic mouse model of moderate Alzheimer׳s disease," Eur. J. Pharmacol., vol. 740, pp. 144–150, Oct. 2014, doi: 10.1016/j.ejphar.2014.06.063.
[v] D. Giuliani et al., "NDP-α-MSH induces intense neurogenesis and cognitive recovery in Alzheimer transgenic mice through activation of melanocortin MC4 receptors," Mol. Cell. Neurosci., vol. 67, pp. 13–21, Jul. 2015, doi: 10.1016/j.mcn.2015.05.004.
[vi] D. A. York, S. Boghossian, and M. Park-York, "Melanocortin activity in the amygdala
influences alcohol intake," Pharmacol. Biochem. Behav., vol. 98, no. 1, pp. 112–119, Mar. 2011, doi: 10.1016/j.pbb.2010.12.010.
