Aging is a complex term to define all the physiological changes accumulated with time that lead organisms to death. Many genes have been related with the control of aging in C. elegans. These include different classes as daf, age, or clk genes. At the biochemical level it has been reported that aging induces oxidative damage and vice versa. Antioxidants have been proved to modulate aging rate in some organisms such as worms, flies and mammals, probably by preventing oxidative damage. Ubiquinone (coenzyme Q) is an ubiquitous lipid antioxidant found in all aerobic organisms studied so far, and the balance between its endogenous content and the dietary uptake modulate life span. We have identified by RNAi silencing, eight genes involved in ubiquinone (Q9) biosynthesis in the nematode C. elegans. These genes are homologues to those described previously in S. cerevisiae and include clk-1
, previously implicated in this biosynthetic pathway, and Y57G11C.11/ coq-3
whose deletion in C. elegans is lethal and leads to sterility. Silenced animals show lower levels of both Q9 and Q8 provided by dietary E. coli strains. C. elegans also contained rhodoquinone (RQ9) and the interference on some of these genes also affects its concentration. Unlike clk-1
mutants, none of the interfered animals accumulated the Q- biosynthetic intermediate demethoxy-Q9 (DMQ9), movement or pharyngeal pumping, were not significantly affected. Q9 levels reverted after diet restitution based on non-interfering E. coli strains. Worms silenced in one of these genes showed an extended life span compared with non- interfered animals, but either movement or pharyngeal pumping was not significantly affected. These results suggest that proteins encoded by genes C24A11.9, F57B9.4, Y57G11C.11, T03F1.2, ZK652.9, K07B1.2, ZC395.2 (clk-1
) and C35D10.4, are involved in Q9 biosynthesis in C. elegans.