Sites of mercury inhibition of amino acid transport in fish gut

In polluted waters, mercury accumulation in the intestine and other tissues of marine and estuarine fish can reach several orders of magnitude above those found in the water column. Entrance of mercury compounds, especially HgCl₂, via food and drink into the lumen of the gut can inhibit the normal absorption of amino acids and sugars.^1-5 When applied as HgCl₂ to the mucosal side of fish intestine, mercury binds strongly to the apical membrane facing the lumen and is transferred at a low rate across the gut epithelium to the blood.^6-8 The site(s) of mercury inhibition of amino acid absorption may be on the luminal face of the apical membrane, intracellular, or on the basolateral membrane facing the interstitial fluid in equilibrium with blood. A combination of these sites is not ruled out. The relative effect of the application of HgCl₂ to the mucosal, and separately, to the serosal sides of the gut during leucine transport was investigated. ¹⁴C-Leucine transfer in toadfish midgut was measured in two sets of Ussing chambers.⁹ The results showed a 70-74% inhibition of net mucosal-to-serosal (M → S) transfer and an 89% inhibition of tissue accumulation when HgCl₂ was on the mucosal side. In the parallel series, when HgCl₂ was applied on the serosal side only, the net mucosal-to-serosal transfer was reduced by 48-52% while tissue accumulation was only slightly below the control. Tissues preloaded with ¹⁴C-leucine were investigated with respect to cell-to-mucosal (→ M) or cell-to-serosal (C → S) efflux. Mucosal HgCl₂ had a minimal and complex inhibitory effect on C → M efflux and no effect on C → S efflux. By contrast, serosal HgCl₂ had no effect on C → M efflux and caused only a weak reduction in C → S efflux. These results indicate that HgCl₂ inhibits amino acid transport mainly by blocking transfer channels at the extracellular face of the apical (mucosal), and to a lesser degree, basolateral (serosal) membrane of the gut epithelium.