Abstract

The essential amino acid histidine performs critical roles in health and disease. These functions are generally attributed to the amino acid itself, but could also be mediated by a positive effect on trace element bioavailability. Mechanistic information regarding the absorption of histidine across the gastrointestinal tract is essential for understanding the interplay between amino acid and mineral nutrients and the implications of these interactions for nutrition and toxicology. Using intestinal brush-border membrane vesicles obtained from freshwater rainbow trout, absorption of histidine over the range 0.78-780 microM: was found to be saturable, with a maximal transport rate (J (max)) of 9.1 +/- 0.8 nmol mg protein(-1) min(-1) and a K (m) (histidine concentration required to reach 50% of this level) of 339 +/- 68 microM: . Histidine uptake was highly specific as 10-fold elevated levels of a variety of amino acids with putative shared transporters failed to significantly inhibit uptake. Elevated levels of D: -histidine, however, impaired uptake of the natural L: -isomer. The presence of "luminal" copper (8.3 microM: ) significantly increased both the J (max) and K (m) of histidine transport. This suggests that chelated copper-histidine species cross the brush-border epithelium through transport pathways distinct from those used by histidine alone.

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