ATP is an excellent energy storage molecule to use as "currency" due to the phosphate groups that link through phosphodiester bonds. These bonds are high energy because of the associated electronegative charges exerting a repelling force between the phosphate groups. A significant quantity of energy remains stored within the phosphate-phosphate bonds. Through metabolic processes, ATP becomes hydrolyzed into ADP, or further to AMP, and free inorganic phosphate groups. The process of ATP hydrolysis to ADP is energetically favorable, yielding Gibbs-free energy of -7.3 cal/mol.[1] ATP must continuously undergo replenishment to fuel the ever-working cell. The routine intracellular concentration of ATP is 1 to 10 uM.[2] Many feedback mechanisms are in place to ensure the maintenance of a consistent ATP level in the cell. The enhancement or inhibition of ATP synthase is a common regulatory mechanism. For example, ATP inhibits phosphofructokinase-1 (PFK1) and pyruvate kinase, two key enzymes in glycolysis, effectively acting as a negative feedback loop to inhibit glucose breakdown when there is sufficient cellular ATP.
Conversely, ADP and AMP can activate PFK1 and pyruvate kinase, serving to promote ATP synthesis in times of high-energy demand. Other systems regulate ATP, such as in the regulatory mechanisms involved in regulating ATP synthesis in the heart. Novel experiments have demonstrated that ten-second bursts called mitochondrial flashes can disrupt ATP production in the heart. During these mitochondrial flashes, the mitochondria release reactive oxygen species and effectively pause ATP synthesis. ATP production inhibition occurs during mitochondrial flashes. During low demand for energy, when heart muscle cells received sufficient building blocks needed to produce ATP, mitochondrial flashes were observed more frequently. Alternatively, when energy demand is high during rapid heart contraction, mitochondrial flashes occurred less often. These results suggested that during times when substantial amounts of ATP are needed, mitochondrial flashes occur less frequently to allow for continued ATP production. Conversely, during times of low energy output, mitochondrial flashes occurred more regularly and inhibited ATP production.[3]
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