Hoyle I ; Handy RD ;

Aquatic Toxicology vol. 72 (1-2)   pp. 147-59, 2005

School of Biological Sciences, University of Plymouth, Drake Circus, Plymouth PL4 8AA, UK.

The trophic transfer and nutritional toxicity of mercury (Hg) in aquatic food chains is well known, but there is limited information on the mechanism of mercury uptake across the gut. In this study, isolated whole gut sacs from rainbow trout were used to identify the regions of the gut involved in Hg absorption, and then perfused intestines were used to investigate Hg uptake. Exposure of whole gut sacs to 100 micromol l(-1) Hg as HgCl2 in the luminal solution caused Hg accumulation primarily in the mucosa (78% or more), with the intact mid and hind gut supporting 59% of the accumulated Hg. Luminal exposure to [Hg] between 0 and 100 micromol l(-1) for 4 h in perfused trout intestines showed a non-linear dose-dependent accumulation with a maximum Hg uptake rate of about 103 nmol g(-1) h(-1), and suggests carrier mediated transport into the gut cells and the blood. Additions of 2 mmol l(-1) amiloride depressed Hg accumulation by the mid and hind gut by 40-50%, whilst additions of the Ca chelator 1 mmol l(-1) EGTA increased Hg levels in the tissue. Symmetrical additions of 10 mmol l(-1) cyanide did not prevent tissue accumulation of Hg, but caused a 3.4-fold decline in net Hg flux to the serosal compartment. We conclude that Hg absorption across the gut is partly carrier mediated and involves both amiloride sensitive, and energy-dependent pathways.

Amiloride ;  Pharmacology ;  Analysis of Variance ;  Animals ;  Biological Transport ;  Drug effects ;  Physiology ;  Comparative Study ;  Dose-Response Relationship ;  Drug ;  Egtazic Acid ;  England ;  Intestines ;  Metabolism ;  Mercury ;  Pharmacokinetics ;  Models ;  Biological ;  Oncorhynchus mykiss ;  Potassium Cyanide ;  Spectrophotometry ;  Atomic ;  Time Factors ;