Macromolecular damage leading to cell, tissue and ultimately organ dysfunction is a major contributor to aging and is induced in large part by intracellular reactive oxygen species (ROS) produced inside cells. Mitochondria play a central role in regulating the rate of macromolecular damage, as they are the principal source of ROS. The mitochondrial complex I, a component of the electron transport chain in mitochondria,  is the major electron entry point for the respiratory chain and thus an important source of ROS in mitochondria. ROS generated by mitochondria target the mitochondrial DNA (mtDNA), and somatic mtDNA mutations have been reported in normal aging, leading to a corresponding decline in the mitochondrial function with age. Although this decline leads to further ROS production, the causal relationship between naturally occurring variations in the mitochondrial genomes leading to correspondingly less or more ROS and macromolecular damage that changes the rate of aging associated organismal decline has remained unexplored. In their new study titled "Relationship between oxidative stress and lifespan in Daphnia pulex", Drs. Benedicth Ukhueduan and Andy Schumpert, both former graduate sudents in the Patel lab, Dr. Eunsuk Kim, former postdoc in the Dudycha lab, and Drs. Rekha Patel and Jeff Dudycha, both professors in the department, used Daphnia as a model organism to explore if the naturally occurring sequence variations in NADH dehydrogenase subunit 5 (ND5), a core protein of the mitochondrial complex I, correlate with a short or long lifespan. They discovered that short-lived Daphnia clones have ND5 variants that correlate with reduced complex I activity, increased oxidative damage, and heightened expression of ROS scavenger enzymes. Their study also establish Daphnia as a unique model system to study natural determinants of lifespan. Congrats!