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Bone marrow transplantation demonstrates that carbonic anhydrase II deficiency limited to bone marrow-derived cells affects ammonium chloride tolerance in mice.

Abstract
Bone marrow transplantation (BMT) in mice was utilized to determine the relative importance of carbonic anhydrase II (CA II) deficiency in blood compared to kidney in the pathogenesis of the ammonium chloride intolerance observed in CA II-deficient mice. "Normal" BMT experiments utilized normal donors and CA II-deficient recipients (NL-->DEF), "reverse" BMT experiments utilized CA II-deficient donors and normal recipients, and control BMT experiments utilized normal mice with a hemoglobin polymorphism (Hbb d/s). Unstressed urinary pH was not significantly altered by normal or reverse BMT, nor was any change induced by control BMT. However, DEF-->NL mice showed markedly altered weight changes when placed on oral ammonium chloride, an effect apparently secondary to dehydration due to decreased water intake. In addition, some CA II-deficient mice have a urinary concentrating defect. Red blood cell and kidney CA II deficiency contribute additively to these effects.
AuthorsL G Biesecker, R P Erickson, R E Tashian
JournalBiochemical medicine and metabolic biology (Biochem Med Metab Biol) Vol. 51 Issue 1 Pg. 61-5 (Feb 1994) ISSN: 0885-4505 [Print] United States
PMID8192918 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S.)
Chemical References
  • Ammonium Chloride
  • Carbonic Anhydrases
Topics
  • Ammonium Chloride (pharmacology)
  • Animals
  • Bone Marrow (metabolism)
  • Bone Marrow Cells
  • Bone Marrow Transplantation (physiology)
  • Carbonic Anhydrases (deficiency, metabolism)
  • Drug Tolerance
  • Hydrogen-Ion Concentration
  • Kidney (metabolism)
  • Mice
  • Mice, Inbred C57BL
  • Mice, Inbred DBA
  • Phenotype
  • Urine (chemistry)

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