Mechanisms of Acute and Chronic Waterborne Nickel Toxicity in the Freshwater Cladoceran, Daphnia magna

Abstract

We present evidence that Mg2+ antagonism is one mechanism for acute toxicity of waterborne Ni to Daphnia magna. Acutely, adult D. magna were exposed to either control or 694 microg Ni L(-1) as NiSO4 in moderately soft water (45 mg L(-1) as CaCO3; background Ni approximately 1 microg Ni L(-1)) for 48 h without feeding. Chronically, adults were exposed to either control or 131 microg Ni L(-1) for 14 days (fed exposure). These concentrations were approximately 65% and 12%, respectively, of the measured 48-h LC50 (1068 microg Ni L(-1)) for daphnid neonates in this water quality. The clearest effect of Ni exposure was on Mg2+ homeostasis, as whole-body [Mg2+] was significantly decreased both acutely and chronically by 18%. Additionally, unidirectional Mg2+ uptake rate (measured with the stable isotope 26Mg) was significantly decreased both acutely and chronically by 49 and 47%, respectively, strongly suggesting that Ni is toxic to D. magna due at least in part to Mg2+ antagonism. No impact was observed on the whole-body concentrations or unidirectional uptake rates of Ca2+ during either acute or chronic Ni exposure, while only minor effects were seen on Na+ and Cl- balance. No acute toxic effect was seen on respiratory parameters, as both oxygen consumption rate (MO2) and whole-body hemoglobin concentration ([Hb]) were conserved. Chronically, however, Ni impaired respiratory function, as both MO2 and [Hb] were significantly reduced by 31 and 68%, respectively. Acutely, Ni accumulation was substantial, rising to a plateau between 24 and 48 h of approximately 15 microg g(-1) wet weight--an increase of approximately 25-fold over control concentrations. Mechanisms of acute toxicity of Ni in D. magna differ from those in fish; it is likely that such mechanistic differences also exist for other metals.

Toxicity of Zinc Dissolved In Saigon River to the Tropical Micro-Crustacean Daphnia Lumholtzi

“…However, the metals at high concentration could induce the impairment on the respiratory function of D. magna (Pane et al, 2003) and inhibit ISSN 2164-7682 2016 the sodium uptake leading to the osmotic imbalance in aquatic animals (Grosell et al, 2002) leading to the energy cost for maintain consequently fecundity reduction. This helped to explain the strong inhibition on reproduction in the exposure to 46 and 75 µg Zn/L (Table 4) which was ever reported elsewhere (Dao et al, 2016).…”

Doğa ve Çiftlik Orkinoslarında (Thunnus thynnus L1758) Tespit Edilen Bazı Elementlerin Kemometrik Sınıfl andırması

“…Nickel (Ni) can do no harm to an organism unless the organism absorbs the divalent nickel ion into its body or the nickel ion is bound strongly enough to a membrane (fish gills) so that the membrane cannot function properly. Ni deficiency in the liver is decreased concentrations of Zn in liver 8,9 . Zinc (Zn) is essential element for aquatic life, for example, it occurs in the enzyme carbonic anhydrase, which catalyses the formation of carbonic acid from carbon dioxide in the blood.…”

Evaluation Of The Biotic Ligand Model For Predicting Metal Bioavailability and Toxicity In SRS Effluents And Surface Waters

“…Toxic mechanisms, and therefore the nature of the toxic sites, may be fundamentally different. For example, nickel acts by a respiratory mechanism in fish (Pane et al, 2003a; but by an ionoregulatory mechanism, inhibition of active Mg 2+ uptake, in daphnids (Pane et al, 2003b), so log K values for protective cations will probably differ. Buffering conditions for pH at the gill surface may also differ substantially between these very different organisms, changing the effective log K BL-H+ or even metal speciation (Playle, 1998).…”