To define the relationships between brain mitochondrial activity and high-energy intermediates in the turtle, brains were frozen in situ at times determined by the reduction-oxidation status of cytochrome a,a3. Increases in brain lactate indicated that transition to anaerobiosis occurred while oxidative reactions were still ongoing during hypoxia and that the signal for anaerobiosis is not the complete failure of mitochondrial electron transfer. Decreases in creatine phosphate (CrP), ATP, ADP, and AMP demonstrate that their consumption exceeded production during hypoxia. CrP decreased further during the following 120 min of anoxia, but ATP, ADP, and AMP were not significantly altered from control values. These data suggest that ATP is not inhibitory to rate-limiting, key glycolytic enzymes such as phosphofructokinase. Calculations indicate that ATP production declined during anoxia. This study indicates that decreased CrP values, decreased ATP production, and high lactate levels do not preclude ion homeostasis and electrical activity of turtle brain and that this brain is protected against lactate or pH damage during anoxia, in contrast to mammalian brain.
|Original language||English (US)|
|Journal||American Journal of Physiology - Regulatory Integrative and Comparative Physiology|
|State||Published - 1984|
ASJC Scopus subject areas
- Physiology (medical)