Title: Sunburn and antioxidants

Key words: UV-A, UV-B, serotonin, prostaglandins, inflammation, sensory nerves, c-fibres, pain-specific,

Date: April 2001

Category: Materia medica

Type: Article

Sunburn and antioxidants

Burnt offerings! Sun worshippers must make a painful sacrifice for their sins. Alison Mitchell explores how human flesh burns

YOU COME inside from a day at the beach, step into the shower, then towel yourself dry and smooth on after-sun lotion. If, like many a holiday-maker, you've spent just a bit too long in the sun, it's not a comfortable experience. The water feels scalding hot, the towel seems to be made of wire wool, and applying lotion is like rubbing salt into an open wound. And if the evening gets cool, don't even think about slipping on a woollen cardigan.

According to Clifford Woolf, a neurobiologist at Harvard Medical School in Boston, these unpleasant symptoms of sunburn are there for your own good. When common sense fails to keep us out of the sun, the body resorts to pain to prevent us from damaging ourselves further. But how exactly does this pain come about after you've finished roasting on the beach? What puts the burn into sunburn?

"Sunburn isn't a burn in the sense of heating skin to a noxious level," says Woolf. At the heart of the matter lies the skin's response to ultraviolet (UV) light. As you slow-cook in the sun, your skin is zapped not only by visible light and heat, but also by two types of UV radiation. UV-A, with wavelengths just shorter than visible violet light, has been linked to skin cancer. But the shorter-wavelength UV-B is most dangerous and causes sunburn-or UV burn as it's known in the trade. UV radiation triggers the production of highly reactive oxygen free radicals in the skin, and these have to be mopped up before they wreak too much havoc.

Lobster look

At the first signs of damage the immune system leaps into action, releasing a cocktail of chemicals to start the cleanup process. This inflammatory mixture, which includes serotonin, prostaglandin-E2 and hydrogen ions, increases blood flow to the areas under attack, delivering immune cells and chemicals to where they are needed. This makes the skin look red, a bit like when you blush, but only the areas that have been exposed. Unlike with cuts and sprains, where the inflammatory response immobilises the injured area with widespread swelling and stiffness until it has healed, the more localised response means you end up with a distinct line where your swimsuit ends.

So it's the body trying to sort out the damage already done that explains the lobster look. But what about the pain that goes with it? This is all down to the skin's sensory nerve fibres, which come in two main flavours. A-fibres, which respond to sensations such as touch, vibration, pressure, temperature or pain, mostly have a very low threshold for activation. They fire off a signal at the slightest provocation. C-fibres, on the other hand, have a much higher activation threshold, and their response generally registers as pain.

Our reaction to something noxious-a hot pan, say-can be divided into two phases, explains Woolf. A rapid, instantaneous pain, mediated by the A-fibres, is followed by a slower but longer-lasting C-fibre pain. Each fibre stretches from the spinal cord to the skin, where it branches to form a number of sensory endings. Whether or not a pain signal is transmitted depends on whether tiny channels in their membranes are open or closed, in most cases to the influx of sodium ions. This is dictated, in turn, by the presence or absence of potentially harmful stimuli.

Woolf's group, in collaboration with Simon Tate at Glaxo Wellcome in Stevenage near London, has studied one of these pain-specific channels, called the tetrodotoxin-resistant (TTX-R) sodium channel, found mainly in the C-fibres. Woolf's team, and others, has discovered that the TTX-R channel is opened by, among other things, hydrogen ions and prostaglandin-E2. This allows sodium ions to flood into the C-fibres, kicking off a pain signal. The fibres also release neuropeptides, which set off a cascade of reactions to draw more blood and water into the affected areas-which is why the frazzled skin is not only red, but a tiny bit swollen too.

But the TTX-R channel is only half of the story. Two years ago, David Julius and colleagues at the University of California in San Francisco identified a channel in the C-fibres called the capsaicin receptor. Capsaicin is the stuff that puts the "hot" in red hot chilli peppers, and, as the receptor's name implies, it responds to this spice. But the receptor's main job, Julius has shown, is to detect painful levels of heat. Whereas some channels open at low temperatures, the capsaicin receptor snaps into action only at the temperatures we register as painful, about 43 C to 45 C, says Julius.

Or at least that's what normally happens. Like the TTX-R channel, the capsaicin receptor can also be opened by the inflammatory cocktail. In sunburnt skin the inflammatory signals cause the receptor to become sensitised, perhaps by a slight tweaking of its shape or by a change in how it passes on its signals. "Its activation threshold could then be lowered to about 35 C", says Julius, "so a much cooler stimulus, such as a tepid shower, would be enough to trigger a pain signal". He speculates that touch receptors might also become sensitised, explaining the tenderness of sunburnt skin. The capsaicin receptor's high activation threshold might also explain why you don't feel any pain while you're actually in the sun: "It is very unlikely the skin would get hot enough to activate the capsaicin receptors directly," says Julius.

But while the hapless holiday-makers are nursing their sore skin, the natives are turning golden brown. Bronzed bodies don't usually burn because melanin, the pigment in tanned and dark skin, prevents UV from penetrating further than the top layer of skin cells. However, tanned skin may heat up more, because it reflects less visible light. "This reinforces the notion that the burn in sunburn is not a heat burn, but an inflammatory burn," says Woolf.

But if you don't fancy spending hours on a sunbed before hitting the beach, help is at hand. According to Bernhard Przybilla and colleagues at the Ludwig Maximilian University in Munich, vitamins C and E also reduce the sunburn reaction. These vitamins are antioxidants, and Przybilla's group believes they soak up oxygen free radicals before they do too much harm- another good reason to eat plenty of salad in the summer. But if greens aren't your thing, Julius says, "aspirin can be quite effective."

Perhaps the best way to avoid any pain is to remember the "shadow rule", suggested by Thomas Downham from the Henry Ford Medical Center in Taylor, Michigan. When your shadow is shorter than your height, he says, the intensity of UV radiation from the sun is more likely to cause sunburn. If you plan to enjoy the sun this summer, hiding in the shade when the shadows are short could just stop you from feeling the burn.

Alison Mitchell is an associate editor at Nature

From New Scientist magazine, vol 163 issue 2197, 31/07/1999, page 26

© Copyright New Scientist, RBI Ltd 2000