Researchers have found a reason to distrust the results of past nematode life span studies with modest effect sizes, even those that controlled for the effects of dietary intake on longevity, a now well-known issue in animal studies that has caused plenty of problems in the past. The researchers have found that light exposure affects the life span of the commonly used Caenorhabditis elegans species of nematode. Their data shows a sizable difference between conditions of permanent light and permanent darkness, but the problem would arise more subtly in comparison between studies where duration, intensity, and type of lighting varied - say, by season, by employee hours, by building fixtures, by nematode housing, and so forth. By the sound of it, this is bad news for near all past life span studies carried out with nematodes, casting doubt on a large amount of exploratory data in the field of aging research.
Historically, the nematode Caenorhabditis elegans was believed to lack the ability to sense light due to the absence of a bona fide photoreceptor system and its original isolation in soil samples. However, recent work in C. elegans has identified the LITE-1 taste receptor homolog as a UV-specific photoreceptor. Interestingly, high-energy UV and blue wavelength light trigger escape behavior and feeding inhibition in C. elegans. In contrast to animals with external pigmentation, the transparent body of nematodes allows light to penetrate their body, making them particularly vulnerable to the mutagenic effects of UV.
We used C. elegans to test whether the photoperiod (the interval in a 24-h period during which an animal is exposed to light) could impact its physiology and lifespan. This is also of special interest since standard laboratory manuals and practices for C. elegans handling completely ignore random exposure to light versus dark. Here, we demonstrate that daily exposure to white light decreases C. elegans lifespan and alters development. Importantly, these effects are not mediated through known photoreceptor pathways or through a proper disruption of circadian rhythms. Our results indicate that the effect of light on C. elegans lifespan is not specific to a particular wavelength of the visible spectrum, but is photon energy dependent.
We find that light exposure causes oxidative stress and induces canonical stress responses. Several long-lived mutants that ectopically activate these stress-responsive pathways are resistant to light stress. Furthermore, we find that treatment of wild-type worms with antioxidants is sufficient to rescue their short lifespan due to light exposure. Such findings strongly invite a reconsideration of the standard methods of C. elegans handling, especially in the context of aging research and stress biology.