We often discuss the importance of the mitochondrial adenine nucleotide exchanger; indeed, many suggest it is rate limiting for oxidative phosphorylation. But its function has no effect on total mitochondrial nucleotide content.
What is your view of the control of total mitochondrial adenine nucleotide content (ATP + ADP + AMP)? Are isolated mitochondria capable of purine biosynthesis?
If mitochondria can only exchange one mitochondrial ATP for one cytosolic ADP, then there is nothing a mitochondrion can do to increase or decrease the sum of mitochondrial ATP+ADP+AMP. This seems paradoxical. Where does a mitochondrion get its initial allocation of adenine nucleotides?
As we know nucleotide (including ATP + ADP + AMP) biosystheis is tightly controlled at gene level, so, mitochondrial levels of adenines is a reflection of their cellular level as suggested above.
But I think flow of adenines (not an increse in content) into mitochondria can be increased with enhanced demand by mitochondrial respiration, aerobic exercise or by starvation etc. as recent researchers suggest.
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