Phosphate reserves
A well-fed adult in the industrialized world consumes and excretes about 1-3 g of phosphorus per day in the form of phosphate (2-6 x 1022 molecules). Per the elemental composition of the "standard man" of 70 kg, phosphorus is 780 g or 1.1% (as 1.52 x 1025 molecules of phosphate).[1] Of this 1.4 g/kg (98 g, 1.9 x 1024 molecules of phosphate) are present in soft tissue with the remainder (1.33 x 1025 molecules of phosphate) in mineralized tissue such as bone and teeth.[2] Only about 0.1% of body phosphate (about 2 x 1022 molecules) circulates in the blood, but this amount reflects the amount of phosphate available to soft tissue cells. Blood plasma contains orthophosphate (as HPO42-) and H2PO4- in the ratio of about 4:1.[2]
The total quantity of ATP in the human body is about 0.1 mole (about 6 x 1022 molecules). This ATP is constantly being broken down into ADP, and then converted back into ATP. At any given time, the total amount of ATP + ADP remains fairly constant. The energy used by human cells requires the hydrolysis of 100 to 150 moles (6 to 9 x 1025 molecules) of ATP daily which is around 50 to 75 kg. Typically, a human will use up their body weight of ATP over the course of the day.[3] This means that each ATP molecule is recycled 1000 to 1500 times daily, or about once every minute.
There are intracellular and extracellular PPi levels in many tissues.
Intracellular phosphate
With the number of cells in the human body of 10-100 trillion or 1013 to 1014, there are approximately 1.9-19.0 x 1010 atoms of phosphorus (1.9 to 19 x 1010 molecules of phosphate) per cell. Some of this, ~6 x 108 molecules can be ATP.
A typical cell volume is 5 x 10-16 m3. If a typical cell was totally liquid water, there would be about 1.7 x 1013 molecules of water present. Then the phosphate concentration would be on the order of 10-3. However, a cell is about twice as dense as liquid water, then perhaps only 50% water yielding 5 x 10-3 for phosphate concentration. As computer simulation has shown the probability of finding a target by diffusion decreases rapidly with distance and becomes <1% when the starting distance exceeds the target's 10-fold radius,[4] which by assumption of a simple spherical volume would put the target's concentration on the order of 10-3.
Although ectonucleotide pyrophosphatase/phosphodiesterase 3 (ENPP3) regulates intracellular PPi concentrations it does not seem to significantly regulate extracellular PPi.[5]
Extracellular phosphate
PPi inhibits hydroxyapatite deposition in bone and cartilage.[5] Many studies have shown that PPi is a potent inhibitor of calcification, bone mineralization, and bone resorption.[6] Human defects in alkaline phosphatase, an enzyme that degrades PPi, lead to an increase in PPi levels and a severe block in skeletal mineralization.[6] Genetic defects in a cell surface ectoenzyme that normally generates extracellular PPi from nucleotide triphosphate cause ectopic mineralization of joints and ligaments and may be associated with spinal ligament ossification in humans.[6]
Bone
During bone resorption high levels of phosphate are released into the ECF as osteoclasts tunnel into mineralized bone, breaking it down and releasing phosphate, that results in a transfer of phosphate from bone fluid to the blood. During childhood, bone formation exceeds resorption, but as the aging process occurs, resorption exceeds formation.
References
- ↑ CRC Handbook of Chemistry and Physics (88th ed.). Boca Raton, Florida: CRC Press. 2007–2008. p. 7-18. Unknown parameter
|editor-in-chief=ignored (help) - ↑ 2.0 2.1 Schwartz MK. "Phosphate metabolism". McGraw-Hill Encyclopedia of Science & Technology (9th ed.). 13: 343–4.
- ↑ Buono MJ, Kolkhorst FW (2001). "Estimating ATP resynthesis during a marathon run: a method to introduce metabolism" (PDF). Adv Physiol Educ. 25 (2): 70–1.
- ↑ Guigas G, Weiss M (2008). "Sampling the Cell with Anomalous Diffusion—The Discovery of Slowness". Biophys J. 94 (1): 90–4. doi:10.1529/biophysj.107.117044. PMID 17827216. Unknown parameter
|month=ignored (help) - ↑ 5.0 5.1 Rutsch F, Vaingankar S, Johnson K, Goldfine I, Maddux B, Schauerte P, Kalhoff H, Sano K, Boisvert WA, Superti-Furga A, Terkeltaub R (2001). "PC-1 nucleoside triphosphate pyrophosphohydrolase deficiency in idiopathic infantile arterial calcification". Am J Pathol. 158 (2): 543–54. PMID 11159191. Unknown parameter
|month=ignored (help) - ↑ 6.0 6.1 6.2