Abstract
Chemically reinforced essential fatty acids (FAs) promise to fight numerous age-related diseases including Alzheimer’s, Friedreich’s ataxia and other neurological conditions. The reinforcement is achieved by substituting the atoms of hydrogen at the bis-allylic methylene of these essential FAs with the isotope deuterium. This substitution leads to a significantly slower oxidation due to the kinetic isotope effect, inhibiting membrane damage. The approach has the advantage of preventing the harmful accumulation of reactive oxygen species (ROS) by inhibiting the propagation of lipid peroxidation while antioxidants potentially neutralize beneficial oxidative species. Here, we developed a model system to mimic the human dietary requirement of omega-3 in Caenorhabditis elegans to study the role of deuterated polyunsaturated fatty acids (D-PUFAs). Deuterated trilinolenin [D-TG(54:9)] was sufficient to prevent the accumulation of lipid peroxides and to reduce the accumulation or ROS. Moreover, D-TG(54:9) significantly extended the lifespan of worms under normal and oxidative stress conditions. These findings demonstrate that D-PUFAs can be used as a food supplement to decelerate the aging process, resulting in extended lifespan.
Highlights
IntroductionThe brain consumes around 20% of oxygen despite making only 2% of body weight
Sensitive to oxidative damage, the brain consumes around 20% of oxygen despite making only 2% of body weight
Together with the thiobarbituric acid reactive substrate (TBARS) assay, these results demonstrate that deuterated polyunsaturated fatty acids (D-polyunsaturated fatty acids (PUFAs)) is sufficient to prevent lipid peroxidation in C. elegans
Summary
The brain consumes around 20% of oxygen despite making only 2% of body weight. The brain is rich in polyunsaturated fatty acids (PUFAs) and oxygen in the lipid bilayer is high reaching millimolar levels (Subczynski and Hyde, 1983). This tissue requires large quantity of ATP to maintain intracellular ion homeostasis resulting in high oxygen uptake. The brain spends a quarter of its energy to maintain and repair lipid membranes damaged from ROS (Brenna and Carlson, 2014). Several studies demonstrated that blocking the production of lipid peroxides can be beneficial to prevent the development of Alzheimer’s disease (AD), Parkinson’s disease, and Huntington’s disease (Huang et al, 1999; Lee et al, 2011; Reed, 2011; Gandhi et al, 2012; Shichiri, 2014; Deas et al, 2016)
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