The dynamics of chronically bioaccumulated Cd in rainbow trout (Oncorhynchus mykiss) during both moderately hard and soft waterborne exposures.

摘要

Aquatic organisms respond to metal exposures by modulating uptake, elimination and detoxification capacity and, therefore, it is difficult to link accumulation within fish to adverse chronic effects. When fish are exposed to sublethal concentrations of metal, physiological responses follow a damage-repair scenario with rapid uptake into the gills followed by transfer via the circulatory system and accumulation into key organs such as the liver and kidney. Anthropogenic sources of cadmium (Cd) arise mainly from mining, smelting, and refining sulphide ores of Zn, Pb and Cu (Norton et al., 1990). The free divalent ion (Cd 2+) is the toxic form of Cd in water. Cd2+competes with calcium ions (Ca2+) for binding sites and transport channels across the basolateral membrane of the gill. Ambient Ca is the primary cation responsible for reduced Cd toxicity to species of trout, during both acute and chronic waterborne exposures. The objective of this research was to examine the dynamics of chronically accumulated Cd within tissues of rainbow trout (Oncorhynchus mykiss) during chronic (one month) sublethal waterborne exposures to Cd (0.75 and 2.0 mug/L) in both moderately hard (140 mg/L as CaCO3) and moderately soft (50 mg/L as CaCO3 ) water. Accumulation was assessed on a tissue (gills, liver and kidney) and subcellular levels. Tissues accumulated Cd in a time- and dose-dependent manner. Results indicate that fish exposed to sublethal Cd concentrations in moderately soft water attained higher amounts of Cd in gills, and more Cd bound to metal-sensitive fractions (mitochondria and proteins) in all tissues in comparison to fish exposed to Cd in moderately hard water. Early mortality and ion-loss may link to accumulation in metal-sensitive fractions (particularly within the gills). However, Cd concentrations in metal-sensitive fractions continued to rise throughout both sublethal exposures suggesting damage-repair mechanisms other than metallothionein are induced, or threshold Cd concentrations in tissues and metal-sensitive fractions associated with adverse effects have not been exceeded. The kidney appeared to be most capable organ to offer protection from Cd accumulation in metal-sensitive fractions, as Cd dissipated from metal-sensitive fractions with time and dose. Also kidneys displayed the highest capacity to induce detoxification of Cd by metallothionein.