Despite early reports, dating back three quarters of a century, of high total CO(2) concentrations in the intestinal fluids of marine teleost fishes, only the past decade has provided some insight into the functional significance of this phenomenon. It is now being recognized that intestinal anion exchange is responsible for high luminal HCO(3)(-) and CO(3)(2-) concentrations while at the same time contributing substantially to intestinal Cl(-) and thereby water absorption, which is vital for marine fish osmoregulation. In species examined to date, the majority of HCO(3)(-) secreted by the apical anion exchange process is derived from hydration of metabolic CO(2) with the resulting H(+) being extruded via a Na(+):H(+) exchange mechanism in the basolateral membrane. The basolateral H(+) extrusion is critical for the apical anion exchange and relies on the Na(+) gradient established by the Na(+)-K(+)-ATPase. This enzyme thereby ultimately fuels the secondary active transport of HCO(3)(-) and Cl(-) by the apical anion exchanger. High cellular HCO(3)(-) concentrations (>10 mmol l(-1)) are required for the anion exchange process and could be the result of both a high metabolic activity of the intestinal epithelium and a close association of the anion exchange protein and the enzyme carbonic anhydrase. The anion exchange activity in vivo is likely most pronounced in the anterior segment and results in net intestinal acid absorption. In contrast to other water absorbing vertebrate epithelia, the marine teleost intestine absorbs what appears to be a hypertonic fluid to displace diffusive fluid loss to the marine environment.