Durk Pearson & Sandy Shaw’s®
Life Extension NewsTM
Volume 15 No. 3 • June/July 2012


Scientists Develop Mitochondria-targeted Antioxidants That Protect Pancreatic Beta-cells Against Oxidative Stress and Improve Insulin Secretion

A recent paper1 reports on experimental benefits of two mitochondria-targeted antioxidants, MitoTempol and Mitoquinone (MitoQ). The researchers exposed pancreatic beta cells to glucotoxic (toxic, high levels of glucose) and glucolipotoxic (high levels of glucose and fats), which result in increased mitochondrial ROS (reactive oxygen species) production, leading to the sort of damage that is found in patients with type 2 diabetes.

MitoTempol or Mitoquinone were shown to prevent the deleterious effects to the pancreatic beta-cells under the glucotoxic and glucolipotoxic conditions, promoting their survival and increasing insulin secretion.

“Mitotempol and Mitoquinone (MitoQ) are two promising mitochondria-targeted antioxidants derived from tempol (an antioxidant nitroxide) and ubiquinone, which are targeted to mitochondria by covalent attachment to a lipophilic [fat loving] triphenylphosphonium cation.”1 The antioxidant MitoTempol (for example) “decreases ROS generation, reduces abdominal fat and the weight gain, decreases blood glucose and normalizes blood insulin and creatinine levels in obese/Zucker rats fed a high fat diet [references given here have been deleted].”1 Moreover, the authors explain, “[p]ancreatic beta-cells are particularly susceptible to destruction by mitochondrial ROS because the expression level of antioxidant enzymes in pancreatic islets is low.”1

We hypothesize that, since hydrogen easily enters mitochondria and has substantial antioxidant effects, especially against the hydroxyl radical, the most toxic type of free radical and one for which no physiological control mechanism has yet been identified, and the potent toxicant peroxynitrite (created by the chemical reaction of superoxide and nitric oxide) might provide benefits similar to mitochondria-targeted antioxidants. Importantly, we note that this hypothesis has NOT yet been experimentally tested. Indeed, the identification of the mechanisms that explain the source of hydrogen’s beneficial effects is still sketchy and in the very early stages. There are no data yet available that compare the effects of hydrogen with mitochondria-targeted antioxidants such as the two described above.

Hence, we have written this up as a thought experiment, that hydrogen, like antioxidants such as those described above that can penetrate mitochondria, may offer protection that improves on the results that have been obtained with antioxidants heretofor in the attempted treatment of oxidative stress arising in mitochondria.

Reference

  1. Lim et al. Mitochondria-targeted antioxidants protect pancreatic beta-cells against oxidative stress and improve insulin secretion in glucotoxicity and glucolipotoxicity. Cell Physiol Biochem 28:873-86 (2011)

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