Metal-Gill Surface Interactions in Rainbow Trout (Oncorhynchus mykiss)
Experiments were conducted on rainbow trout to analyze: 1) the impact on gill function of cadmium (Cd⁺⁺) as compared to the effects of copper (Cu⁺⁺) and low pH (H⁺), 2) the metal binding characteristics of the external gill surface, and 3) modifications in metal binding activity of the gills associated with chronic exposure to low Ca⁺⁺ water or aluminum (Al).
Short-term exposure (24 h) to equimolar (6.5 μmol‧Lˉ¹)Cd⁺⁺, Cu⁺⁺, or H⁺ (pH 4.8) resulted in the disruption of transepithelial ion exchange in trout, confirming the surface activity of Cu⁺⁺ and H⁺, and characterizing the impact of Cd⁺⁺ on gill function. The effects of each metal were different from one another with respect to specific site of action, rapidity of action, and persistence of the disturbance. Furthermore, Cu⁺⁺ and 11⁺ had only minor effects on Ca⁺⁺ balance and major effects on Na⁺ balance whereas the reverse was the case for Cd⁺⁺, with water hardness ([Ca⁺⁺]) having a fundamentally different role to play in the toxicity of Cd⁺⁺ compared to Cu⁺⁺.
Analysis of metal-gill surface interactions, using an in vitro methodology, revealed that metal binding kinetics were related predominantly to the charge of the metal. The gills had the highest affinity for lanthanum (La⁺⁺⁺) and AI, intermediate affinity for Ca⁺⁺ and Cd⁺⁺, and the lowest for Cu⁺⁺ and H⁺. All metals, with the exception of Cu⁺⁺, would inhibit the binding of Ca⁺⁺ to the gills. These metals were ranked, in decreasing ability to act as Ca⁺⁺-antagonists at the gill surface, as follows: AI, La⁺⁺⁺, Cd⁺⁺ and H⁺ then Cu⁺⁺. Although the binding affinity, and, to some extent, the competitiveness of these metals was correlated with charge, metal toxicity was correlated with neither the metal charge nor the affinity of the metal-gill surface interaction.
The gill micro-environment was found to be capable of responding in an adaptive fashion to environmental stressors (low Ca⁺⁺ water or elevated AI). Modifications of the gill, in response to the reduction of water Ca⁺⁺, resulted in a significant increase in the Ca⁺⁺ binding affinity and capacity of the external gill surface. Furthermore, chronic exposure to elevated AI induced a prophylactic response by the gill micro-environment, resulting in a significant suppression of the surface activity of AI manifested as an enhanced resistance to the ionoregulatory and hematological impact of Al exposure.