ArticleMechanisms of ageing and development2009
The effect of different ubiquinones on lifespan in Caenorhabditis elegans.
Article in Mechanisms of ageing and development, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 42 citations in OpenAlex.
- The treatment of primary CoQ deficiency requires the targeting of multiple pathogenic mechanisms.Communications medicine · 2025Article
- The marine environmental microbiome mediates physiological outcomes in host nematodes.BMC biology · 2024Article
- Review
- We are all aging, and here's why.Aging medicine (Milton (N.S.W)) · 2022Review
- Animal Models of Coenzyme Q Deficiency: Mechanistic and Translational Learnings.Antioxidants (Basel, Switzerland) · 2021Review
- Human geroprotector discovery by targeting the converging subnetworks of aging and age-related diseases.GeroScience · 2020Article
- The Paradox of Coenzyme QNutrients · 2019Review
- The Comparative Biology of Mitochondrial Function and the Rate of Aging.Integrative and comparative biology · 2018Article
- N-acetylcysteine and vitamin E rescue animal longevity and cellular oxidative stress in pre-clinical models of mitochondrial complex I disease.Molecular genetics and metabolism · 2018Article
- Activation of DAF-16/FOXO by reactive oxygen species contributes to longevity in long-lived mitochondrial mutants in Caenorhabditis elegans.PLoS genetics · 2018Article
- Cell Biology of the Mitochondrion.Genetics · 2017Review
- Mitochondrial and cytoplasmic ROS have opposing effects on lifespan.PLoS genetics · 2015Article
- Invertebrate models for coenzyme q10 deficiency.Molecular syndromology · 2014Article
- Mitohormesis: Promoting Health and Lifespan by Increased Levels of Reactive Oxygen Species (ROS).Dose-response : a publication of International Hormesis Society · 2014Article
- Novel interactions between mitochondrial superoxide dismutases and the electron transport chain.Aging cell · 2013Article
- Oxidative stress mechanisms underlying Parkinson's disease-associated neurodegeneration in C. elegans.International journal of molecular sciences · 2013Review
- Article
- ROS in aging Caenorhabditis elegans: damage or signaling?Oxidative medicine and cellular longevity · 2012Review
- Branched-chain amino acids, mitochondrial biogenesis, and healthspan: an evolutionary perspective.Aging · 2011Review
- Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
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.
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