Abstract

Brush border membrane vesicles (BBMVs) were prepared from the kidneys of rainbow trout exposed acutely (72 h; 13,380 μg Ni L − 1 ), chronically (11 months; 289 μg Ni L − 1 ), or chronically and acutely, to waterborne nickel (Ni). Uptake of 63Ni into renal BBMVs was temperature-dependent and fitted a two component kinetic model composed of a saturable, Michaelis–Menten component prominent at lower Ni concentrations, and a moderate linear diffusive component apparent at higher Ni concentrations. Chronic Ni exposure reduced the permeability of the BBM to Ni, evidenced by a significantly reduced slope of the linear diffusive component of BBMV uptake. Efflux of Ni from 63Ni-loaded renal BBMVs was not significantly altered by acute Ni challenge. Both Ca 2+ and Mg 2+ inhibited uptake of Ni into renal BBMVs when present at a molar ratio to Ni of 1000 : 1. Mg 2+-induced inhibition, however, was concentration-dependent and significant in BBMVs prepared from chronically Ni-acclimated fish at far lower molar ratios of 100 and 10 to 1. The data suggest that subtle, long-term modulation of membrane structure and function in the rainbow trout may be a compensatory response to chronic waterborne Ni exposure. Additionally, the data challenge the assumptions of constancy of the physiological parameters underlying physiologically based approaches to modeling metal toxicity. Such approaches are currently employed to derive water quality criteria for some metals.

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