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Volume 16 No. 7 • August 2013


Glycine Protects Brain Tissues UnderHypoxic (Oxygen Deficient) Conditions

The amino acid glycine, which among other things, is part of the regulatory pathways for sleep and has been shown to improve sleep quality, has been reported in a recent paper1 to protect the brain against energetic disturbances arising under hypoxic (oxygen deficient) conditions. We think that glycine may be a useful supplement for neurological protection in those with sleep apnea.

Glycine is being used as a therapy for ischemic stroke2 and has been reported to increase the lifespan of cortical neurons under hypoxic conditions.3 A new paper1 now explains a mechanism underlying this protective effect that has advanced glycine to patient treatment in the clinic. Hypoxia in brain tissues was induced in rats by ligation of the common carotid artery. The resulting hypoxia reduced respiratory control in brain cortex mitochondria from 7.7 ±0.5 to 4.5 ±0.3, indicating impaired respiration. Preliminary oral administration of glycine at 40 mg/kg 4 times with 1 hour intervals almost completely prevented this decrease.

The authors1 report that published data “suggest that hypoxia is associated with activation of peroxidation processes in the brain tissue.” The authors, therefore, measured hydrogen peroxide accumulation in mitochondria after short-term exposure to hypoxia and found that the oxidation of succinate was accompanied by a rapid generation of hydrogen peroxide. Hydrogen peroxide formation was significantly lower after incubation of brain cortex slices with glycine. Oxidative phosphorylation (energy generation in mitochondria) was preserved in mitochondria in the presence of 5 mM glycine in the incubation medium. The researchers suggest, therefore, that mitochondria are the target of glycine in the brain cortex under hypoxic conditions. This is particularly interesting because of the fact that substances, such as many antioxidants, that are protective under the oxidative conditions induced by hypoxia frequently are unable to enter mitochondria and are, therefore, unable to provide much, if any, protection there. (Hydrogen is one antioxidant that does reach mitochondria.)

References

  1. Selin et al. Mechanism underlying the protective effect of glycine in energetic disturbances in brain tissues under hypoxic conditions. Bull Exp Biol Med. 153(1):44-7 (2012).
  2. Gusev et al. Neuroprotective effects of glycine for therapy of acute ischaemic stroke. Cerebrovas Dis. 10(1):49-60 (2000).
  3. Zhao et al. GABA and glycine are protective to mature but toxic to immature rat cortical neurons under hypoxia. Eur J Neurosci. 22(2):289-300 (2005).

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