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Waterborne cadmium and nickel impact oxidative stress responses and retinoid metabolism in yellow perch.

Aquatic toxicology (Amsterdam, Netherlands) (2014-06-11)
Michel A Defo, Louis Bernatchez, Peter G C Campbell, Patrice Couture
ABSTRACT

In this experiment, we studied the transcriptional and functional (enzymatic) responses of yellow perch (Perca flavescens) to metal stress, with a focus on oxidative stress and vitamin A metabolism. Juvenile yellow perch were exposed to two environmentally relevant concentrations of waterborne cadmium (Cd) and nickel (Ni) for a period of 6 weeks. Kidney Cd and Ni bioaccumulation significantly increased with increasing metal exposure. The major retinoid metabolites analyzed in liver and muscle decreased with metal exposure except at high Cd exposure where no variation was reported in liver. A decrease in free plasma dehydroretinol was also observed with metal exposure. In the liver of Cd-exposed fish, both epidermal retinol dehydrogenase 2 transcription level and corresponding enzyme activities retinyl ester hydrolase and lecithin dehydroretinyl acyl transferase increased. In contrast, muscle epidermal retinol dehydrogenase 2 transcription level decreased with Cd exposure. Among antioxidant defences, liver transcription levels of catalase, microsomal glutathione-S-transferase-3 and glucose-6-phosphate dehydrogenase were generally enhanced in Cd-exposed fish and this up-regulation was accompanied by an increase in the activities of corresponding enzymes, except for microsomal glutathione-S-transferase. No consistent pattern in antioxidant defence responses was observed between molecular and biochemical response when fish were exposed to Ni, suggesting a non-synchronous response of antioxidant defence in fish exposed to waterborne Ni. There was a general lack of consistency between muscle transcription level and enzyme activities analyzed. The overall findings from this investigation highlight the usefulness of transcriptional and biochemical endpoints in the identification of oxidative stress and vitamin A metabolism impairment biomarkers and the potential use of multi-level biological approaches when assessing environmental risk in fish.

MATERIALS
Product Number
Brand
Product Description

Sigma-Aldrich
Raney®-Nickel, W.R. Grace and Co. Raney® 2800, slurry, in H2O, active catalyst
Nickel, foam, 150x150mm, thickness 1.6mm, bulk density 0.45g/cm3, porosity 95%, 95%
Sigma-Aldrich
Cadmium, powder, −100 mesh, 99.5% trace metals basis
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Nickel, nanopowder, <100 nm avg. part. size, ≥99% trace metals basis
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Cadmium, granular, 30-80 mesh, ≥99%
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Cadmium, granular, ≥99%, 5-20 mesh
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Raney®-Nickel, W.R. Grace and Co. Raney® 2400, slurry, in H2O, active catalyst
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Nickel, foil, thickness 0.125 mm, ≥99.9%
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Nickel, powder, <150 μm, 99.99% trace metals basis
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Nickel, wire, diam. 0.25 mm, ≥99.9%
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Nickel, foil, thickness 0.5 mm, 99.98% trace metals basis
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Nickel, wire, diam. 0.5 mm, ≥99.99% trace metals basis
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Nickel, rod, 100mm, diameter 3.3mm, 99.99+%
Nickel, rod, 100mm, diameter 16mm, 99.99+%
Nickel, wire reel, 10m, diameter 0.01mm, as drawn, 99.98%
Cadmium, foil, 4mm disks, thickness 0.25mm, as rolled, 99.99+%
Nickel, foil, not light tested, 100x100mm, thickness 0.01mm, 99.95%
Nickel, wire reel, 250m, diameter 0.25mm, annealed, 99%
Nickel, wire reel, 1m, diameter 1.0mm, hard, 99.98%
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Nickel, broken cathode squares, 1000g, max. size 50mm, 99.8%
Nickel, tube, 1000mm, outside diameter 6.5mm, inside diameter 5.5mm, wall thickness 0.5mm, hard, 99.5%