Suntanning & Cells
Previously, the effect of UV radiation on skin as well as the relationships and pathways of eumelanin production have been analyzed. But what is the relationship between these two? Why does UV radiation from the sun sometimes lead to a suntan, and not a sunburn? This module goes into detail regarding the specific effect of the enzyme tyrosinase, and how its abundance and reactivity can ultimately improve the skin’s ability to produce eumelanin at a heightened rate as a tanning response.
Tyrosinase
Let’s recall the eumelanin production process. It consists of many different genes and their associated proteins, all of which are essential to produce eumelanin. One of those key proteins is tyrosinase. Tyrosinase is the essential enzyme that kickstarts the process by which tyrosine is eventually converted into the eumelanin polymer. Based on the knowledge that eumelanin is responsible for the shade of human skin color, it can be deduced that for a suntan to occur, the rate of eumelanin production must increase. By doing a case study of tyrosinase, there are one of two ways an increase in eumelanin production is a result of sun exposure; one where the sun exposure affects tyrosinase’s ability to be used more readily, and one where the sun exposure results in an elevated tyrosinase production.
Increasing Reactivation
Taking a closer look at the enzyme tyrosinase and its function, it is noticeable that it can only be used in the eumelanin production pathway once. Once it is used, it becomes deactivated. However, diacylglycerol (DAG) creates protein kinase (PKC), and PKC is able to reactivate a used tyrosinase enzyme, which then renders it capable of further assisting in eumelanin production. When UV radiation from the sun is exposed to skin cells, these skin cells become damaged, which results in the release of DAG from the cell’s membrane. This then stimulates PKC production, which in turn will elevate the amount of PKC. This heightened amount of PKC is then capable of reactivating tyrosinase enzymes more frequently, thus resulting in increased eumelanin production.
Increasing Concentration
The other process involves the production of more tyrosinase. Similarly to how PKC is produced at an elevated rate when UV radiation penetrates the skin, UV radiation can also stimulate production of the enzyme pro-opiomelanocortin (POMC), which in turn breaks down and signals MC1R. As addressed in an earlier section, MC1R is a transmembrane protein that eventually leads to the production of cAMP. When there is excess cAMP production, this can cause an increased rate at which the tyrosinase gene is transcribed, thus increasing the rate at which translation can form tyrosinase proteins, thus producing an elevated amount of tyrosinase than what regularly occurs. This increased number of tyrosinase proteins present is then capable of producing a heightened amount of eumelanin.
Fitzpatrick Scale
So whether the tyrosinase enzyme’s productivity and efficiency is increased, or whether it itself is increased in concentration, either way would theoretically lead to an increase in eumelanin production, thus darkening the shade of affected skin. However, it should be noted that not all people tan at the same rate either. Some individuals, such as those with Type 1 skin on the Fitzpatrick scale, actually are unable to produce eumelanin at all. Due to a nonfunctioning MC1R gene, MC1R is inactive within their skin, and thus no eumelanin is produced. On the other end of the scale, those with Type 6 skin already produce so much eumelanin regularly that an increase is hardly, if at all noticeable. So the amount of eumelanin that can be produced is extremely dependent on the individual scale, and fluctuates for everyone.
