2,3 Biphosphoglycerate

[ace_inhibitor111]

---

Members do not see this ad.

Hi, I just wanted to clarify: I know 2,3 BPG reduces oxygen affinity in hemoglobin causing it to release oxygen in active tissues. However, I read online that while 2,3 BPG increases with decreasing pH, 2,3 BPG mutase, which creates 2,3 BPG, is inactivated at low pH's. How is this possible? Thank you.

 

[Morsetlis]

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1220500/pdf/10477270.pdf

An initial response to acute hypoxia is hyperventilation, which causes respiratory alkalosis. If this alkalosis is prevented, the usual accumulation of 2,3-BPG is prevented. This result implicates blood pH in the control of 2,3-BPG concentration. The importance of blood pH in controlling 2,3-BPG concentration is also supported by a number of studies. Increases in pH above the usual physiological value result in 2,3-BPG accumulation, while decreases result in depletion. This pH-dependence is dramatic; the steady-state concentration of 2,3-BPG in glycolysing erythrocytes decreases from its usual steady-state value of E7 mM to zero with a decrease of only 0.4 pH unit.

Deoxygenation of erythrocytes leads to an increase in intracellular pH of 0.07±0.14 pH unit due to deoxygenated Hb (deoxy-Hb) having a higher affinity for protons (acting as a base) than oxygenated Hb (oxy-Hb).

Hypoxia -> Hyperventilation -> decreased PCO2 -> Respiratory alkalosis -> lowered [H+] -> stimulation of 2,3-BPG Mutase -> increase in 2,3-BPG -> O2 dissociation from Hb
Hypoxia -> Increased deoxy-Hb -> lowered [H+] ... etc

Rest assured that if an MCAT question EVER talks about 2,3-BPG Mutase, they will provide all the information you would need.

 

[ace_inhibitor111]

Thanks for the help. Yeah, I know it is probably too specific but it has been bugging me for a while.