Osteoclasts in bone tissue are particularly rich in carbonic anhydrase II, and a
ID: 37608 • Letter: O
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Osteoclasts in bone tissue are particularly rich in carbonic anhydrase II, and a proper functioning enzyme is critical to the development of healthy tissue. In order for proper bone development to occur, the osteoclast must acidify the bone-resorbing compartment. Also involved in this acidification are several transporters: a Na+/H+, exchanger, a Cl-/HCO3- exchanger and the Na+K+ATPase, which exchanges Na+ and K+ ions. (An exchanger is a protein or protein complex located in the cell membrane which transports one ion in one direction and the second ion in the other direction simultaneously.) A partial diagram of the osteoclast is shown in Figure 3.1. Fill in the blanks in the diagram indicating the roles of carbonic anhydrase II and the exchangers in the acidification of the bone-resorbing compartment. Include the reactants and products of the appropriate intracellular reaction(s) and note in which direction each ion is transported in the osteoclast.Explanation / Answer
the role of carbonic anhydrase 2 in the establishment of the acidity of the bone resorbing compartment in osteoclasts is - Osteoclasts resorb bone by attaching themselves to the bone surface and then secreting protons into an extracellular compartment formed in the intermediate region that is, between the osteoclast and bone surface. This proton or acidic secretion is necessary for bone mineral solubilization and the digestion of organic bone matrix by acid proteases (bone solubilizing enzyme).
The primary mechanism that is responsible for acidification of the osteoclast-bone interface is vacuolar H+-adenosine triphosphatase (ATPase) coupled with Cl- conductance localized to the ruffled membrane. Where, Carbonic anhydrase II (CAII) provides the proton source for extracellular acidification by H+-ATPase and the HCO3- source for the HCO3-/Cl- exchanger. Whereas some other transporters are also responsible for the bone resorption process, and some others are essential for pH regulation in the osteoclast.
The HCO3-/Cl- exchanger, in association with CAII, is the major transporter for maintenance of normal intracellular pH. An Na+/H+ antiporter may also contribute to the recovery of intracellular pH during early osteoclast activation. Once this mechanism has been rendered inoperative, another conductive pathway translocates the protons and modulates cytoplasmic pH. Inward-rectifying K+ channels may also be involved by compensating for the external acidification due to H+ transport. These different effects of transport processes, either on bone resorption or pH homeostasis, increase the number of possible sites for pharmacological intervention in the treatment of metabolic bone diseases.
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