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Title: K+-H+ exchange and volume homeostasis in brown adipose tissue mitochondria. Author: DiResta DJ, Kutschke KP, Hottois MD, Garlid KD. Journal: Am J Physiol; 1986 Oct; 251(4 Pt 2):R787-93. PubMed ID: 3766779. Abstract: K+-H+ exchange activity in hamster brown adipose tissue mitochondria is activated following depletion of matrix Mg2+ with the divalent cation ionophore A23187. Quinine inhibits K+-H+ exchange reversibly with an I50 of 22 microM, whereas mild treatment with N,N'-dicyclohexylcarbodiimide (DCCD) inhibits this activity irreversibly. In an attempt to label and identify the K+-H+ antiporter protein, brown adipose tissue mitochondria were incubated with [14C]DCCD and subjected to denaturing polyacrylamide gel electrophoresis and fluorography. We observed a labeled band of relative mol wt, 78,000, which satisfies criteria established in rat liver mitochondria for the identification of this carrier (W. H. Martin et al., J. Biol. Chem. 259: 2062-2065, 1984). Thus Mg2+ and quinine each protect the K+-H+ exchanger against both inhibition and binding by DCCD. Volume homeostasis in brown adipose tissue mitochondria, as in other mitochondria, requires a balance between K+ influx and efflux. We propose that regulation of the K+-H+ antiporter, the primary K+ efflux mechanism, plays a major role in this process.[Abstract] [Full Text] [Related] [New Search]