The effects of dietary selenomethionine on tissue-specific accumulation and toxicity of dietary arsenite in rainbow trout (Oncorhynchus mykiss) during chronic exposure.

The interactive effects of different doses of dietary selenium [as selenomethionine; 1.8 µg g-1 (control), 10 µg g-1 and 40 µg g-1 diet] on the toxicity of dietary arsenic [as arsenite (As3+); 80 µg As per g diet] were investigated in rainbow trout over an exposure period of 30 days. Fish fed with As3+ alone showed an increased hepatic lipid peroxidation (LPO) and a concomitant decline in cellular redox potential (determined as GSH:GSSG) in the liver tissue relative to the control fish. Interestingly, fish fed with low (10 µg g-1) or high (40 µg g-1) concentration of dietary selenomethionine in combination with As3+ showed an even higher degree of hepatic LPO and a further decrease in GSH : GSSG molar ratio relative to the fish treated with As3+ alone. Our study also revealed that exposure to dietary selenomethionine (both at low and high levels) resulted in significantly higher levels of arsenic in target tissues (liver, kidney, and muscle) relative to fish treated with As3+ alone. Similarly, the synchrotron-based X-ray fluorescence imaging analysis also suggested a dose-dependent increase in the co-localization of arsenic and selenium in the brain of fish co-treated with dietary As3+ and selenomethionine. These observations suggested that selenomethionine facilitated arsenic deposition in the brain and likely in other tissues, possibly via bio-complexation. Overall, our findings indicated that elevated dietary selenomethionine can increase the tissue-specific accumulation and toxicity of As3+ in fish during chronic dietary exposure.

A FTIRM study of the interactive effects of metals (zinc, copper and cadmium) in binary mixtures on the biochemical constituents of the gills in rainbow trout (Oncorhynchus mykiss).

We employed Fourier Transform Infrared Microspectroscopy to examine, in situ, the effects of waterborne Cu, Cd and Zn, alone and in binary mixtures, during acute exposure on the integrity of major lipid and protein constituents of the gill of a model teleost species, rainbow trout (Oncorhynchus mykiss). Our findings demonstrated that acute exposure to metals, both individually and in binary mixture, resulted in the degradations of various components of proteins and lipids in the gill tissue. Generally, when comparing the effects of individual metals, Cu was found to induce the maximum adverse effects followed by Cd and Zn, respectively. Among the binary metal-mixture combinations, Cu and Cd produced additive effects on the degradation of major proteins and lipid moieties, whereas the co-exposure of Zn with Cd or Cu elicited ameliorative effects, indicating antagonistic (less than additive) interactions between Zn and Cd or Cu in the rainbow trout gill. Overall, the present study demonstrates that FTIRM can be a useful tool to gain novel mechanistic insights into the biochemical changes induced by metals in the fish gill, which could influence the overall toxicity of metals to fish.

Distribution and speciation of zinc in the gills of rainbow trout (Oncorhynchus mykiss) during acute waterborne zinc exposure: Interactions with cadmium or copper.

We utilized micro X-ray fluorescence imaging (µ-XFI) and micro X-ray absorption near-edge spectroscopy (µ-XANES), which are both synchrotron-based techniques to investigate Zn distribution profile, its co-localization patterns with Ca, S, and Fe and speciation in the gills of rainbow trout (RBT). Fish (~100 g) were exposed to acutely toxic levels of waterborne Zn alone and in combination with waterborne Cd or Cu for 24 h (each at 1 × 96 h LC50). Gill sections were prepared and analyzed at the VESPERS beamline of the Canadian Light Source. The primary lamellae of the fish gill were found to be the primary area of Zn accumulation. These regions also correspond to the zones of mitochondria rich cells localization in fish gills, supporting the putative roles of these cells in metal uptake. Zn was also found to predominantly co-localize with Ca and S, but not with Fe, indicating the roles of Ca and S in intracellular Zn handling. Zn distribution in the gill was markedly reduced during co-exposure to Cd, but not to Cu, suggesting a competitive interaction between Zn and Cd for uptake. The speciation of Zn in the gill was dominated by Zn-phosphate, Zn-histidine and Zn-cysteine species; however, the interactions of Zn with Cd or Cu resulted in the loss of Zn-cysteine. Overall, our findings provide important novel insights into the interactions of Zn, Cd and Cu in the fish gill, which may ultimately help to explain the mechanisms underlying the acute toxicity of these metals in binary mixture to fish.