Melanin: The Chemistry of Skin Colour

Human skin comes in a continuous range of shades, from very pale to very dark, and almost all of that variation comes down to one class of pigment: melanin. The same pigments colour hair and the iris of the eye, darken skin in the sun, and form freckles. Melanin is also one of nature’s most effective sunscreens. Its chemistry is unusual — it isn’t a single molecule with a neat structure, but a tangled polymer that chemists are still working to describe fully.

Where melanin is made

Melanin is produced in specialised cells called melanocytes, which sit in the bottom layer of the epidermis (the outer layer of skin). Inside each melanocyte, melanin is made in small membrane-bound packages called melanosomes. The melanocyte then passes these packages through branching extensions into the surrounding skin cells (keratinocytes), where they gather over the nucleus like a tiny parasol, shielding DNA from sunlight.

An important point: people of all skin colours have roughly the same number of melanocytes per area of skin. Differences in skin colour come from how much melanin each melanocyte makes, which type, and how large and widely spread the melanosomes are. Darker skin tends to have larger, more numerous and more evenly distributed melanosomes.

From tyrosine to pigment

Melanin starts with the amino acid tyrosine (see amino acids). The key enzyme is tyrosinase, a copper-containing enzyme that uses molecular oxygen to oxidise tyrosine in two steps:

1. Tyrosine → L-DOPA (a hydroxyl group is added to the benzene ring, making a catechol — the same catechol unit found in dopamine and adrenaline).
2. L-DOPA → dopaquinone (the two –OH groups are oxidised to C=O groups).

Dopaquinone is highly reactive, and what happens next decides which type of melanin forms.

Eumelanin: brown to black

If little sulfur is around, dopaquinone curls up on itself: its amine group attacks the ring to form a second, five-membered ring. After further oxidation steps, this gives indole units — mainly 5,6-dihydroxyindole (DHI) and 5,6-dihydroxyindole-2-carboxylic acid (DHICA). These link together in many different ways to form eumelanin, a dark brown to black polymer.

Pheomelanin: red to yellow

If the amino acid cysteine is available, its thiol group (–SH) adds to dopaquinone first, creating sulfur-containing intermediates (cysteinyldopas). These form ring structures containing both sulfur and nitrogen, called benzothiazines, which polymerise into pheomelanin, a reddish-yellow pigment.

Which pathway dominates is controlled by signals to the melanocyte — especially a receptor called MC1R. When MC1R is strongly activated, cells make more eumelanin; when it’s less active (as with many variants common in people with red hair), they make more pheomelanin. Most people have a mixture of both pigments in their skin and hair.

A polymer without a clear formula

Most biological molecules — proteins, DNA, starch — have a well-defined repeating structure. Melanin doesn’t. Its building blocks link at different positions, in different ratios and with different degrees of oxidation. The result is a heterogeneous, insoluble material whose structure is still debated. Current models describe eumelanin as small flat sheets of linked indole units stacked on top of each other, like tiny pieces of graphite, which then clump into larger particles.

That disordered structure is actually the key to how melanin works.

How melanin protects against UV

Sunlight contains ultraviolet radiation, which carries enough energy per photon to damage DNA directly — for example by linking neighbouring thymine bases together — and to generate reactive oxygen species. Melanin protects in several ways:

1. Broad absorption. Most coloured molecules absorb a narrow band of wavelengths. Eumelanin’s messy mix of structures means it absorbs across the whole UV and visible range, with absorption rising towards shorter, more damaging wavelengths. That’s why it looks brown-black rather than a specific colour.
2. Harmless energy dumping. After absorbing a photon, eumelanin converts almost all of the energy into heat within a tiny fraction of a second, instead of passing it on to nearby molecules or emitting it as light. Its fluorescence is extremely weak — a sign that the energy is being dissipated safely.
3. Antioxidant action. Melanin can mop up free radicals and reactive oxygen species produced by UV.
4. Physical shielding. The melanosome “caps” over each nucleus block light before it reaches DNA.

Pheomelanin is less protective. It absorbs less strongly, and when UV hits it, it can actually generate reactive oxygen species. This helps explain why people with red hair and fair skin burn easily and have a higher risk of skin cancer.

Why skin tans

Tanning is the skin’s response to UV damage. It happens in two stages:

• Immediate pigment darkening, within minutes to hours: existing melanin is oxidised and redistributed, causing a greyish-brown darkening that fades quickly.
• Delayed tanning, after about two to three days: DNA damage in skin cells triggers them to release signalling molecules (including α-MSH, a hormone that activates MC1R). Melanocytes respond by making more tyrosinase, producing more eumelanin, and passing on more melanosomes.

A tan is therefore a sign that DNA damage has already happened. A typical tan offers only modest protection — roughly equivalent to a low-SPF sunscreen — and doesn’t prevent the damage that leads to ageing and skin cancer.

Skin colour, sunlight and vitamin D

There’s an evolutionary balancing act in skin colour. Dark skin protects against UV damage and against the breakdown of folate, a B vitamin needed for DNA synthesis and healthy pregnancy. But UV-B is also needed to make vitamin D in the skin (see vitamin D chemistry). Near the equator, where UV is intense all year, dark skin protects folate and still allows enough vitamin D. At high latitudes, with weak winter sunlight, lighter skin lets more UV-B through to make vitamin D. This is the leading explanation for why the world’s range of skin colours correlates so strongly with latitude.

Freckles, albinism and grey hair

• Freckles are small patches where melanocytes make more eumelanin in response to sunlight; they’re common in people with certain MC1R variants and fade in winter.
• Albinism usually results from mutations that stop melanin production — most commonly in the gene for tyrosinase. Without melanin, skin, hair and eyes lack pigment, and vision is affected because melanin is also needed for the normal development of the retina.
• Vitiligo is different: melanocytes in patches of skin are destroyed, usually by the immune system, leaving white patches.
• Grey hair occurs as melanocyte stem cells in hair follicles decline with age. Hair grows without pigment; it looks grey or white because the keratin scatters light (see keratin and hair). Hydrogen peroxide building up in follicles may also play a role by interfering with melanin production.

Melanin beyond the skin

Melanin-like pigments are everywhere in nature: in the ink of squid and cuttlefish (sepia), the black spots on bananas, the darkening of cut apples, and the black skin of some fungi. In fruit browning, an enzyme related to tyrosinase (polyphenol oxidase, also copper-containing) oxidises phenolic compounds when cells are cut and exposed to air — a close cousin of melanin chemistry. Lemon juice slows browning because its low pH and its ascorbic acid interfere with the enzyme and reverse the first oxidation (see vitamin C chemistry).

Neuromelanin, a related dark pigment, is found in parts of the brain rich in dopamine; its loss is a hallmark of Parkinson’s disease.

Common misconceptions

• “Darker skin has more melanocytes.” The number is similar; activity and melanosome size differ.
• “A tan protects you from sunburn.” Only modestly, and the tan itself is a response to DNA damage.
• “Melanin is one molecule.” It’s a varied, disordered polymer of two main types.
• “People with dark skin can’t get skin cancer or need no sunscreen.” Risk is lower but not zero.

Key takeaways

• Melanin is made in melanocytes from tyrosine by the copper enzyme tyrosinase.
• Eumelanin (brown–black, from indole units) and pheomelanin (red–yellow, sulfur-containing) differ in chemistry and protective power.
• Melanin absorbs broadly across the UV and visible and converts the energy to heat, shielding DNA.
• Tanning is a delayed response to DNA damage; skin colour reflects a balance between UV protection and vitamin D production.

To learn more about how light and molecules interact, read how we see: retinal and a single double bond.