Resveratrol at Low Doses Shown to Improve Mitochondrial Function

Resveratrol at Low Doses Shown to Improve Mitochondrial Function

A low dose of the natural antioxidant resveratrol can improve mitochondrial function and induce cellular reprogramming, researcher say in a new study.

Researchers believe the compound might be a treatment candidate for mitochondrial diseases.

The study reporting the finding, “Low dose resveratrol ameliorates mitochondrial respiratory dysfunction and enhances cellular reprogramming,” was published in the journal Mitochondrion.

Mitochondria exist in nearly all cells (except red blood cells) and create more than 90% of the energy the body needs. When they fail, as happens in mitochondrial diseases, cell injury and death follow. That can produce a range of symptoms, usually in the heart, brain, muscles, and lungs.

Several drugs and supplements with cell-supporting properties have been studied to treat mitochondrial diseases — including coenzyme Q10, vitamin C, creatine, and sodium dichloroacetate — but clinical trials have not provided any convincing support for their use as frontline treatments.

Oxidative stress from free radicals has been reported to induce mitochondrial dysfunction and cell damage, and resveratrol — an antioxidant (meaning it counteracts oxidative stress) — has been shown to be preventive. It also reportedly has anti-aging, anti-inflammatory, and anti-tumor properties, and has protective effects on the brain, heart, and circulatory system.

The compound is mainly found in peanuts, berries, and in the skin of grapes.

A research team investigated the effects of resveratrol in human skin cells (fibroblasts) from three patients with mitochondrial disease. In addition, skin cells from a healthy person were studied for possible toxic effects of resveratrol.

Treatment with a low dose of resveratrol improved all the cells’ mitochondrial function, compared to placebo treatment. It also increased the efficiency of cellular reprogramming . (Cellular reprogramming is converting a somatic cell type — such as skin cell — to an induced pluripotent stem cell. The stem cells then have the potential to transform into any other somatic cell in the body.)

The study showed that the lowest-used dose of resveratrol increased cell growth, while the highest dose dramatically induced cell death, indicating that the compound could have side effects in humans in high doses.

Further research is needed to determine whether a low dose of resveratrol could benefit other cell types, such as neurons and heart cells, the researchers said.

”But our results highlight the potential of resveratrol as a new therapeutic drug candidate for the treatment of mitochondrial diseases,” the authors wrote.


  1. GIorgio Terziani says:

    J Physiol Pharmacol. 2011 Jun;62(3):287-93.
    Cellfood™ improves respiratory metabolism of endothelial cells and inhibits hypoxia-induced reactive oxygen species (ros) generation.
    Ferrero E1, Fulgenzi A, Belloni D, Foglieni C, Ferrero ME.
    Author information
    Endothelial mitochondria, the major site of ATP generation, modulate the intracellular dynamics of reactive oxygen species (ROS), which, in turn, control endothelial function. Adequate oxygen (O(2)) supply is required by endothelial cells (EC). Both hypoxia and hyperoxia may favor the overproduction of ROS leading to oxidative stress, mitochondrial damage and endothelial dysfunction. We investigated the capability and mechanisms of Cellfood™ (CF), an antioxidant compound, to modulate O(2) availability and mitochondrial respiratory metabolism and to regulate ROS generated by hypoxia in EC in vitro. Human umbilical vein endothelial cells (HUVEC) and ECV-304 were evaluated for the O(2) consumption using a Clark’s electrode. The O(2) consumption rate rose, during the first minutes after CF addition and was associated with increase in mitochondrial oxidative capacity and good cell viability. Similar behaviours were observed when EC were exposed to CF for up to 8 days. The O(2) consumption increased and was accompanied by both intracellular rise of ATP and maintainment of LDH concentration. Hypoxia-induced ROS generation was significantly inhibited by CF, through the up-regulated expression of MnSOD, an anti-oxidant responsible for mitochondrial function preservation. The EC hypoxic response is mediated by the hypoxia master regulator HIF-1alpha whose activation was attenuated by CF, in concomitance with MnSOD up-regulation. Our results suggest a role for CF in improoving respiratory metabolism and in activating anti-oxidant mechanisms in EC, thus preserving endothelial function.
    PMID: 21893688
    [PubMed – indexed for MEDLINE] Free full text

  2. Alexandra Andersson, PhD says:

    Dear Jim,
    I wish I could give you specific doses that make sense, but the concentrations used to treat specific cells in the research study, are not comparable to the oral doses used in supplements or food.
    Until more information comes up, it is best to follow the current recommendations regarding doses of resveratrol.

    Kind regards
    Alexandra Andersson
    BioNews Services

  3. Richard Head says:

    The idea of antioxidants is somewhat murky. We have a umber of studies showing that use of supplemental antioxidants decreases the signals from the damaged mitochondria and blocks the normal repair process. It seems that a certain level of free radicals etc. are necessary. It maybe that as we age and as we have more mito damage that some an mount of antioxidant would decrease the overload of signals that can trigger of inflammatory reactions as well as repair. (speculation on my part). There is also the question as to whether these antioxidant supplements are absorbed.

    One study showed that use of resveratrol and other antioxidants during a group exercising 5 day a week for 6 weeks versus a control showed damage increased in the antioxidant group but the exercise allowed increase in function of the mito in the controls. See my blog site- Our energy production and the one on exercise for details.

Leave a Comment

Your email address will not be published. Required fields are marked *