ИСТИНА

Mitochondria-bound isoforms I and II of hexokinase are shown to utilize ATP which is produced from ADP and phosphate inside mitochondria to be electrophoretically pumped by ATP4-/ADP3- antiporter and porin to the outer surface of outer mitochondrial membrane. On this surface, ATP and glucose are converted by mitochondria-bound hexokinases I or II to ADP and glucose 6-phosphate. Then ADP is pumped to mitochondrial matrix by the same antiporter. Such an ADP cycling results in moderate decrease in mitochondrial membrane potential and, as a consequence, in strong inhibition of reactive oxygen species (ROS) formation by respiratory complexes I and III. Glucose-6-phosphate is transformed (via “glycolytic” metabolic chain) to pyruvate, which can be used to initiate the Krebs cycle (respiration) or to form lactate (glycolysis). In the latter case, the ATP-producing respiration cooperates with glycolysis in contrast to old dogma that respiration inhibits glycolysis (the Pasteur effect) or, alternatively, glycolysis inhibits respiration (the Crabtree effect). The above relationships are found to be inherent to any studied tissues of mouse embryo or adult naked mole rat but are absent in adult mouse liver. In brain of adult mouse, the antioxidant effect of mitochondria-bound hexokinase was reported by Galina and coworkers.