Zinc toxicity

About: Zinc toxicity is a research topic. Over the lifetime, 727 publications have been published within this topic receiving 34583 citations. The topic is also known as: zinc poisoning.

Uptake and partitioning of zinc in Lemnaceae.

Abstract: Macrophytes provide food and shelter for aquatic invertebrates and fish, while also acting as reservoirs for nutrients and trace elements. Zinc accumulation has been reported for various Lemnaceae species. However, comparative accumulation across species and the link between zinc accumulation and toxicity are poorly understood. Morphological distribution and cellular storage, in either bound or soluble form, are important for zinc tolerance. This study shows differences in the uptake and accumulation of zinc by three duckweed species. Landoltia punctata and Lemna minor generally accumulated more zinc than Lemna gibba. L. minor, but not L. gibba or L. punctata, accumulated greater concentrations of zinc in roots compared to fronds when exposed to high levels of zinc. The proportion of zinc stored in the bound form relative to the soluble-form was higher in L. minor. L. punctata accumulated greater concentrations of zinc in fronds compared to roots and increased the proportion of zinc it stored in the soluble form, when exposed to high zinc levels. L. gibba is the only species that significantly accumulated zinc at low concentrations, and was zinc-sensitive. Overall, internal zinc concentrations showed no consistent correlation with toxic effect. We conclude that relationships between zinc toxicity and uptake and accumulation are species specific reflecting, among others, zinc distribution and storage. Differences in zinc distribution and storage are also likely to have implications for zinc bioavailability and trophic mobility.

Influence of dissolved organic matter on acute toxicity of zinc to larval fathead minnows (Pimephales promelas).

Abstract: We conducted laboratory toxicity tests in support of the development of a biotic ligand model (BLM) to predict acute toxicity of zinc (Zn) to fathead minnows (Pimephales promelas). To test the effect of dissolved organic matter (DOM) on Zn toxicity, we exposed larval fathead minnows to Zn in water containing elevated concentrations of dissolved organic carbon (DOC) in 96-h static-renewal toxicity tests. We tested DOM isolated from four surface waters: Cypress Swamp, Delaware; Edisto River, South Carolina; Suwannee River, Georgia; and Wilmington, Delaware, wastewater treatment effluent. The DOM isolates from the Edisto River and Wilmington wastewater treatment effluent contained elevated concentrations of NaCl (20-110x control NaCl) due to the use of a Na+-exchange resin to remove Ca2+ and Mg2+ during the DOM isolation process. Therefore, we also performed Zn toxicity tests in which we added up to 20 mM NaCl to exposure solutions containing Cypress Swamp and Suwannee River DOM. A threshold concentration of 11 mg DOC/L was needed to decrease Zn toxicity, after which the 96 h Zn LC50 was positively correlated with DOC concentration. Elevated NaCl concentrations did not alter Zn toxicity in the presence of DOM. In conjunction with data from other studies with fish and invertebrates, results of this study were used to calibrate Version 2.1.1 of the Zn BLM. BLM-predicted LC50s for our exposure waters containing elevated DOM concentrations were within the range of acceptable deviation relative to the observed LC50s (i.e., 0.5-2x observed LC50s); however, BLM-predicted LC50s for our exposure waters containing < 1 mg DOC/L were 2-3x lower than the observed LC50s (i.e., the BLM over-predicted the toxicity). Therefore, the current composite-species BLM for Zn could be improved for fathead minnows if that species were modeled separately from the other species used to calibrate Version 2.1.1.

Mortality, accumulation, and distribution of zinc in the gill system of the dogfish following zinc treatment.

Abstract: Besides being an essential element, Zn has been shown to be toxic to aquatic organisms Acute lethalities of Zn salts to teleosts have been reported, but few data regarding Zn toxicity to elasmobranchs can be found To evaluate the effect of Zn on elasmobranchs and to compare the data with those on teleosts this paper studies Zn toxicity and the accumulation of the metal in the gills of the dogfish Scyliorhinus canicula exposed to 180 and 80 ppM of zinc

Potassium attenuates zinc-induced death of cultured cortical astrocytes.

Abstract: Transient global ischemia induces CA1 hippocampal neuronal death without astrocyte death, perhaps mediated in part by the toxic translocation of zinc from presynaptic terminals to postsynaptic neurons. We tested the hypothesis that cellular depolarization, which occurs in the ischemic brain due to increased extracellular potas- sium and energy failure, might contribute to astrocyte resistance to zinc-induced death. We previously reported that neurons in mixed cortical neuronal-astrocyte cultures were more vulnerable to a 5-15-min exposure to Zn 2 than astrocytes in the same cultures. In the present report, we show that (1) neurons in isolation or in conjunction with astro- cytes were 2-3-fold more sensitive to a 15-min nondepolarizing Zn 2 exposure than are glia; (2) KCl-induced depolarization attenuated glial vulnerability to zinc toxicity but potentiated neuronal vulnerability to zinc toxicity; (3) Zn 2 -induced glial death was attenuated by T-type Ca 2 channel blockade, as well as compounds that increase NAD levels; and (4) both astrocytic 65 Zn 2 accumulation and the increase in astrocytic (Zn 2 )i induced by Zn 2 exposure were also attenuated by depolarization or T-type Ca 2 chan- nel blockers. Zn 2 -induced cell death in astrocytes was at least in part apoptotic, as caspase-3 was activated, and the caspase inhibitor Z-Val-Ala-Asp-fluoromethylketone partially attenuated Zn 2 -induced death. The levels of peak (Zn 2 )i achieved in astro- cytes during this toxic nondepolarizing Zn 2 exposure (250 nM) were substantially greater than those achieved in neurons (40 nM). In glia, exposure to 400 MZ n 2 induced a 13-mV depolarization, which can activate T-type Ca 2 channels. This Zn 2 - induced astrocyte death, like neuronal death, was attenuated by the addition of pyru- vate or niacinamide to the exposure medium. © 2004 Wiley-Liss, Inc.