HGCL2 INHIBITION OF NUTRIENT TRANSPORT IN TELEOST FISH SMALL-INTESTINE

  • 1 January 1981
    • journal article
    • research article
    • Vol. 216  (1) , 70-76
Abstract
Mediated D-glucose and cycloleucine uptakes by killifish [Fundulus heteroclitus] intestinal slices and everted sacs were reduced in a dose-and time-dependent manner by HgCl2 exposure, but nonmediated components of nutrient uptake were not affected. Transport processes in intestinal slices from seawater and fresh water-adapted fish exhibited identical sensitivities to HgCl2. The inhibitory effects of mucosal plus serosal exposure (slices) were no greater than the effects of mucosal exposure alone (sacs), indicating that primary inhibitory sites were on the brush border membrane of the tissue. One to 5 min slice exposures (which caused substantial inhibition of nutrient transport) did not affect cellular water or electrolyte levels (indirect measures of Na,K-ATPase activity). With brush border membrane vesicles from killifish and flounder [Pseudopleuronectes americanus] small intestine, HgCl2 affected only the Na-dependent component of D-glucose uptake. Vesicle Na permeability was not increased by HgCl2 exposure. Kinetic studies with killifish slices and flounder vesicles indicated that both Km and Vmax for glucose transport were affected by HgCl2. HgCl2 evidently blocks intestinal nutrient transport by interacting directly with brush border membrane transport proteins; multiple sites on these proteins are probably affected.

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