The effect of different ubiquinones on lifespan in Caenorhabditis elegans

Ubiquinone (UQ, Coenzyme Q, CoQ) transfers electrons from complexes I and II to complex III in the mitochondrial electron transport chain. Depending on the degree of reduction, UQ can act as either a pro- or an antioxidant. Mutations disrupting ubiquinone synthesis increase lifespan in both the nematode (clk-1) and the mouse (mclk-1). The mutated nematodes survive using exogenous ubiquinone from bacteria, which has a shorter isoprenyl tail length (UQ(8)) than the endogenous nematode ubiquinone (UQ(9)). The mechanism underlying clk-1s increased longevity is not clear. Here we directly measure the effect of different exogenous ubiquinones on clk-1 lifespan and mitochondrial function. We fed clk-1 engineered bacteria that produced UQ(6), UQ(7), UQ(8), UQ(9) or UQ(10), and measured clk-1s lifespan, mitochondrial respiration, ROS production, and accumulated ROS damage to mitochondrial protein. Regardless of dietary UQ, clk-1 animals have increased lifespan, decreased mitochondrial respiration, and decreased ROS damage to mitochondrial protein than N2. However, clk-1 mitochondria did not produce less ROS than N2. The simplest explanation of our results is that clk-1 mitochondria scavenge ROS more effectively than wildtype due to the presence of DMQ(9). Moreover, when compared to other dietary quinones, UQ(10) further decreased mitochondrial oxidative damage and extended adult lifespan in clk-1.