THE CHLORIDE CELL:Structure and Function in the Gills of Freshwater Fishes

  • Steve F. Perry
    Department of Biology, University of Ottawa, Ottawa, 30 Marie Curie, Ontario K1N 6N5, Canada

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<jats:p>▪ Abstract  This review focuses on the structure and function of the branchial chloride cell in freshwater fishes. The mitochondria-rich chloride cell is believed to be the principal site of trans-epithelial Ca<jats:sup>2+</jats:sup>and Cl<jats:sup>−</jats:sup>influxes. Though currently debated, there is accruing evidence that the pavement cell is the site of Na<jats:sup>+</jats:sup>uptake via channels linked electrically to an apical membrane vacuolar H<jats:sup>+</jats:sup>-ATPase (proton pump).</jats:p><jats:p>Chloride cells perform an integral role in acid-base regulation. During conditions of alkalosis, the surface area of exposed chloride cells is increased, which serves to enhance base equivalent excretion as the rate of Cl<jats:sup>−</jats:sup>/HCO<jats:sub>3</jats:sub><jats:sup>−</jats:sup>exchange is increased. Conversely, during acidosis, the chloride cell surface area is diminished by an expansion of the adjacent pavement cells. This response reduces the number of functional Cl<jats:sup>−</jats:sup>/HCO<jats:sub>3</jats:sub><jats:sup>−</jats:sup>exchangers.</jats:p><jats:p>Under certain conditions that challenge ion regulation, chloride cells proliferate on the lamellae. This response, while optimizing the Ca<jats:sup>2+</jats:sup>and Cl<jats:sup>−</jats:sup>transport capacity of the gill, causes a thickening of the blood-to-water diffusion barrier and thus impedes respiratory gas transfer.</jats:p>

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