Lipid Peroxidation and Mitochondrial Dysfunction in Alzheimer's and Parkinson's Diseases: Role of Natural Products as Cytoprotective Agents

Fernández-Moriano, Carlos; González-Burgos, Elena

doi:10.1002/9783527803781.ch6

Cited by 1 publication

(1 citation statement)

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“…Further, the mitochondria contain a high prevalence of lipids vulnerable to peroxidation (such as anionic cardiolipin, phosphatidylethanolamine, and phosphatidylcholine; [ 74 ]. Lipid peroxidation is generally initiated when a sufficiently reactive (i.e., thermodynamically and kinetically competent) free radical (hydroxyl radical) abstracts a bis-allylic hydrogen atom from a methylene group [ 75 ]; consequently, this process is propagated by unstable, adjacent lipid radicals (alkoxyl and peroxyl) [ROOH + Fe 2+ → ROO . + Fe 3+ + H + ] [ 76 , 77 ].…”

Section: Discussionmentioning

confidence: 99%

The mitochondria-targeted antioxidant MitoQ, attenuates exercise-induced mitochondrial DNA damage

et al. 2020

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High-intensity exercise damages mitochondrial DNA (mtDNA) in skeletal muscle. Whether MitoQ - a redox active mitochondrial targeted quinone - can reduce exercise-induced mtDNA damage is unknown. In a double-blind, randomized, placebo-controlled design, twenty-four healthy male participants consisting of two groups (placebo; n = 12, MitoQ; n = 12) performed an exercise trial of 4 x 4-min bouts at 90–95% of heart rate max. Participants completed an acute (20 mg MitoQ or placebo 1-h pre-exercise) and chronic (21 days of supplementation) phase. Blood and skeletal muscle were sampled immediately pre- and post-exercise and analysed for nuclear and mtDNA damage, lipid hydroperoxides, lipid soluble antioxidants, and the ascorbyl free radical. Exercise significantly increased nuclear and mtDNA damage across lymphocytes and muscle ( P < 0.05), which was accompanied with changes in lipid hydroperoxides, ascorbyl free radical, and α-tocopherol ( P < 0.05). Acute MitoQ treatment failed to impact any biomarker likely due to insufficient initial bioavailability. However, chronic MitoQ treatment attenuated nuclear ( P < 0.05) and mtDNA damage in lymphocytes and muscle tissue ( P < 0.05). Our work is the first to show a protective effect of chronic MitoQ supplementation on the mitochondrial and nuclear genomes in lymphocytes and human muscle tissue following exercise, which is important for genome stability.

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