title: Effects of chronic waterborne nickel exposure on growth, ion homeostasis, acid-base balance, and nickel uptake in the freshwater pulmonate snail, Lymnaea stagnalis.
abstract: The freshwater pulmonate snail, Lymnaea stagnalis, is the most sensitive aquatic organism tested to date for Ni. We undertook a series of experiments to investigate the underlying mechanism(s) for this observed hypersensitivity. Consistent with previous experiments, juvenile snail growth in a 21-day exposure was reduced by 48% relative to the control when exposed to 1.3 μg l(-1) Ni (EC20 less than the lowest concentration tested). Ca(2+) homeostasis was significantly disrupted by Ni exposure as demonstrated by reductions in net Ca(2+) uptake, and reductions in Ca(2+) concentrations in the hemolymph and soft tissues. We also observed reduced soft tissue [Mg(2+)]. Snails underwent a significant alkalosis with hemolymph pH increasing from 8.1 to 8.3 and hemolymph TCO2 increasing from 19 to 22 mM in control versus Ni-exposed snails, respectively. Unlike in previous studies with Co and Pb, snail feeding rates were found to be unaffected by Ni at the end of the exposure. Snails accumulated Ni in the soft tissue in a concentration-dependent manner, and Ni uptake experiments with (63)Ni revealed a biphasic uptake profile - a saturable high affinity component at low exposure concentrations (36-189 nM) and a linear component at the high exposure concentrations (189-1,897 nM). The high affinity transport system had an apparent Km of 89 nM Ni(2+) and Vmax of 2.4 nmol g(-1)h(-1). This equates to a logK of 7.1, significantly higher than logK's (2.6-5.2) for any other aquatic organisms evaluated to date, which will have implications for Biotic Ligand Model development. Finally, pharmacological inhibitors that block Ca(2+) uptake pathways in snails did not inhibit Ni uptake, suggesting that the uptake of Ni does not occur via Ca(2+) uptake pathways. As with Cu and Pb, the exact mechanism for the significant disruption in Ca(2+) homeostasis and reduction in juvenile snail growth remains unknown.
authors.affiliation: Department of Biology, University of Saskatchewan, Saskatoon, SK, Canada. Electronic address: som.niyogi@usask.ca.
authors.forename: Som
authors.initials: S
authors.lastname: Niyogi
authors.affiliation: Department of Zoology, University of British Columbia, Vancouver, BC, Canada.
authors.forename: Kevin V
authors.initials: KV
authors.lastname: Brix
authors.affiliation: RSMAS, University of Miami, Miami, FL, USA.
authors.forename: Martin
authors.initials: M
authors.lastname: Grosell
mesh_terms: D000136:Acid-Base Equilibrium / Q000187:drug effects; D000818:Animals; D002118:Calcium / Q000032:analysis; D005618:Fresh Water; D006706:Homeostasis / Q000187:drug effects*; D007477:Ions / Q000378:metabolism; D008195:Lymnaea / Q000737:chemistry / Q000187:drug effects* / Q000254:growth & development; D008274:Magnesium / Q000032:analysis; D009532:Nickel / Q000378:metabolism* / Q000633:toxicity*; D014874:Water Pollutants, Chemical / Q000378:metabolism* / Q000633:toxicity*
chemical_list: D007477:Ions; D014874:Water Pollutants, Chemical; D009532:Nickel; D008274:Magnesium; D002118:Calcium
keywords: Chronic toxicity; Growth; Ion homeostasis; Nickel; Snail; Uptake kinetics