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Intracellular pH regulation in isolated trout gill mitochondrion-rich (MR) cell subtypes: Evidence for Na(+)/H(+) activity. Comparative biochemistry and physiology. Part A, Molecular & integrative physiology [Comp Biochem Physiol A Mol Integr Physiol] Journal article

 
Parks SK, Tresguerres M, Galvez F, Goss GG 
Intracellular pH regulation in isolated trout gill mitochondrion-rich (MR) cell subtypes: Evidence for Na(+)/H(+) activity. [JOURNAL ARTICLE]
Comp Biochem Physiol A Mol Integr Physiol 2009 Oct 23.


We have studied intracellular pH (pH(i)) recovery in isolated trout gill mitochondrion-rich (MR) cells following acidification by the NH(4)Cl pre-pulse technique. Within a mixed MR cell population, one cell type displayed Na(+)-independent pH(i) recovery while the other cell type lacked a Na(+)-independent pH(i) recovery. Cells displaying Na(+) independent recovery exhibited a significantly higher buffering capacity compared to cells lacking Na(+)-independent pH(i) recovery. Cells displaying Na(+) independent recovery were identified as PNA(+) (peanut lectin agluttinin binding) MR cells while those unable to recover were identified as PNA(-) (non-peanut lectin agluttinin binding) MR cells. Therefore, recovery from acidification in the absence of Na(+) provides a direct functional marker for PNA(+) and PNA(-) MR cells. Re-addition of Na(+) to acidified cells resulted in a transient pH(i) recovery in both cell types. This event was abolished by amiloride (500microM) but it was insensitive to phenamil (50microM). The phorbol ester PMA (1microM) potentiated the Na(+) induced pH(i) recovery suggesting that activation by PKC is required for continuous Na(+)/H(+) exchanger activity in trout gill MR cells. This study is the first functional description of pH(i) recovery in trout gill MR cells and provides insight into a putative cellular signaling mechanism that may control pH(i) regulation in the gill epithelium.



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