EXPERIMENTS that go according to plan can be useful. But the biggest scientific advances often emerge from those that do not. Such is the case with a study just reported in the Proceedings of the National Academy of Sciences. When they began it, Hector DeLuca of the University of Wisconsin, Madison, and his colleagues had been intending to examine the effects of ultraviolet (UV) light on mice suffering from a rodent version of multiple sclerosis (MS). By the project’s end, however, they had in their hands two substances which may prove valuable drugs against the illness.

Multiple sclerosis is an autoimmune disease. This means it is caused by a victim’s immune system turning on and destroying parts of his own body. In the case of MS the targets of these attacks, which may continue for years, are the fatty sheaths that insulate nerve cells and thus help nervous impulses to propagate. People suffering from MS are often weakened, and sometimes physically disabled by it, and may also become blind.

What drives the immune system to behave in this way remains mysterious, but in the 1970s researchers uncovered a promising clue when they noticed that MS is rarer near the equator than it is at high latitudes. The first hypothesis proposed to explain this observation was that vitamin D (a substance created by sunlight’s action on precursor molecules in the skin) might be helping to prevent MS. That made sense, since those living in the tropics receive more sunlight than do those in temperate zones. Sadly, follow-up experiments failed to support the notion. Those experiments did, though, lead Dr DeLuca to discover that the preventive effect is associated with a particular sort of sunlight—UV with a wavelength of between 300 and 315 nanometres (billionths of a metre).

His latest experiment was intended to dig deeper into this observation, by using this type of light to irradiate mice that had been injected with chemicals known to cause the rodent equivalent of MS. In a preliminary study he and his colleagues therefore shaved the backs of 12 of these mice and exposed them to UV of the appropriate wavelength every day for a month. To be useful, an experiment like this needs controls with which its results can be compared. Dr DeLuca devised three of these. In one, he applied one of six types of sunscreen to a dozen other shaved mice before exposing them to the ultraviolet rays. To another dozen he applied the sunscreen but not the ultraviolet. And a final 12, though also shaved, were neither exposed to UV nor slathered with sunscreen. He then monitored all four groups for signs of murine multiple sclerosis, such as loss of tail tone, unsteady gait and limb paralysis,

When the experiment began, he and his colleagues expected that the disease would progress more slowly in the experimental group than in the control groups, and that its rate of progress in all three control groups would be the same, since any effect of exposure to ultraviolet would be negated by the sunscreen. But that was not what happened. Instead, three of the six types of sunscreen served to suppress the disease’s progression by themselves—that is, even in animals not exposed to UV. Indeed, one of them, Coppertone, was as effective at doing so as ultraviolet light alone.

In light of this Dr DeLuca and his colleagues carried out further experiments, which confirmed the initial findings. They also studied the ingredients lists of the three protective sunscreens and tested each of the compounds therein, one at a time, on other batches of mice. This revealed that two of these compounds, homosalate and octisalate, were particularly effective at keeping the rodent version of multiple sclerosis in check.

Why these particular substances suppress MS remains to be discovered. Dr DeLuca suspects that it has to do with their ability to inhibit production of cyclooxygenase, an enzyme commonly found in the lesions characteristic of multiple sclerosis. But regardless of the mechanism, if homosalate and octisalate, or other molecules similar to them, can suppress the progression of the disease in people as effectively as they do in rodents it will be a signal example both of the role of serendipity in science and of the crucial importance of doing proper controls.