Mechanism underlying the protective effect of glycine in energetic disturbances in brain tissues under hypoxic conditions.

Glycine stabilizes energetics of brain mitochondria under conditions of brain hypoxia in vivo modeled by ligation of the common carotid artery in rats. Hypoxia reduced respiratory control in brain cortex mitochondria from 7.7 ± 0.5 to 4.5 ± 0.3. Preliminary oral administration of glycine almost completely prevented this decrease. In both in vitro models of hypoxia, similar phosphorylation disturbances were detected in both cortical slices and isolated brain mitochondria; they were effectively prevented by glycine. Hypoxia activates H(2)O(2) generation in mitochondrial suspension. The process is significantly reduced in the presence of 5 mM glycine. It is concluded that both in the model of hypoxia in vivo and during in vitro modeling of hypoxia in cortical slices and mitochondria, glycine acts as a protector inhibiting generation of reactive oxygen species in mitochondria and preventing energetics disturbances in brain mitochondria.