HgCl2 inhibition of nutrient transport in teleost fish small intestine.
Mediated D-glucose and cycloleucine uptakes by killifish 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 sea water 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-adenosine triphosphatase activity). With brush border membrane vesicles from killifish and flounder small intestine, HgCl2 affected only the Na-dependent component of D-glucose up-take. 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. Taken together, these findings indicate that HgCl2 blocks intestinal nutrient transport by interacting directly with brush border membrane transport proteins; the kinetic data indicate that multiple sites on these proteins are probably affected.
D000596:Amino Acids / Q000378:metabolism*; D000818:Animals; D003515:Cycloleucine / Q000378:metabolism*; D004573:Electrolytes / Q000378:metabolism; D005399:Fishes / Q000378:metabolism*; D005947:Glucose / Q000378:metabolism*; D007408:Intestinal Absorption / Q000187:drug effects*; D007421:Intestine, Small / Q000187:drug effects; D008628:Mercury / Q000494:pharmacology*; D008871:Microvilli / Q000378:metabolism; D010042:Ouabain / Q000494:pharmacology
D000596:Amino Acids; D004573:Electrolytes; D003515:Cycloleucine; D010042:Ouabain; D008628:Mercury; D005947:Glucose