What is the location and function of chloride cells?

Chloride Cell

Location: In marine bony fishes the body fluids are hypotonic in relation to the surrounding medium having an osmotic pressure only about one-third to the sea water. Thus they have the problem of losing much water by exosmosis. If happens, then the solutes of the body fluids becomes too ouch concentrated and the cell will die. To overcome this problem some special secretory chloride cells are developed in gills of the fishes.

Functions: These cells excrete the excess salts from the gills of the fishes. Salts if excreted more than the level, may be reabsorbed by the gills to maintain the osmotic concentration of the body fluids.

The mitochondria-rich chloride cell is believed to be the principal site of trans-epithelial Ca²⁺ and Cl⁻ influxes. Though currently debated, there is accruing evidence that the pavement cell is the site of Na+ uptake via channels linked electrically to an apical membrane vacuolar H+-ATPase (proton pump).

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⁻/HCO₃⁻ 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⁻/HCO₃⁻ exchangers.

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 Ca2+ and Cl- influxes. Though currently debated, there is accruing evidence that the pavement cell is the site of Na+ uptake via channels linked electrically to an apical membrane vacuolar H(+)-ATPase (proton pump). 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-/HCO3- 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-/HCO3- exchangers. Under certain conditions that challenge ion regulation, chloride cells proliferate on the lamellae. This response, while optimizing the Ca2+ and Cl- transport capacity of the gill, causes a thickening of the blood-to-water diffusion barrier and thus impedes respiratory gas transfer.