Researchers from Columbia University in New York have found that short-sleeping fruit fly mutants shared the feature of sensitivity to acute oxidative stress, and concluded that sleep facilitates antioxidant processes. In a study published in PLoS Biology, the researchers reasoned that if sleep were required for a core function of health, animals that sleep significantly less than usual should share a defect in that core function. They examined a diverse group of short-sleeping Drosophila mutants and found that they indeed shared a common defect: they were all sensitive to acute oxidative stress. Oxidative stress results from excessive levels of free radicals that can damage cells and lead to organ dysfunction. Toxic free radicals, or reactive oxygen species, can accumulate in cells because of normal metabolism and environmental damage. If the function of sleep is to defend against oxidative stress, increasing sleep should increase resistance to oxidative stress. The effects of experimental pharmacological and genetic manipulations support this hypothesis. Finally, the authors proposed that, conversely, oxidative stress might regulate sleep. Consistent with this hypothesis, they found that reducing oxidative stress in the brain by overexpressing antioxidant genes reduced the amount of sleep. Taken together, these results point to a bidirectional relationship between sleep and oxidative stress; that is, sleep is important for defending the body against oxidative stress, and oxidative stress helps induce sleep. This work is relevant to human health because sleep disorders are associated with many diseases that are also associated with oxidative stress, such as Alzheimer, Parkinson and Huntington diseases. Sleep loss could make individuals more sensitive to oxidative stress and subsequent disease; conversely, pathological disruption of the antioxidant response could also lead to loss of sleep and associated disease pathologies.