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.

Bioavailability models for predicting acute and chronic toxicity of zinc to algae, daphnids, and fish in natural surface waters.

Abstract: Bioavailability models predicting acute and/or chronic zinc toxicity to a green alga (Pseudokirchneriella subcapitata), a crustacean (Daphnia magna), and a fish (Oncorhynchus mykiss) were evaluated in a series of experiments with spiked natural surface waters. The eight selected freshwater samples had varying levels of bioavailability modifying parameters: pH (5.7-8.4), dissolved organic carbon (DOC, 2.48-22.9 mg/L), Ca (1.5-80 mg/L), Mg (0.79-18 mg/L), and Na (3.8-120 mg/L). In those waters, chronic zinc toxicity (expressed as 10% effective concentrations [EC10]) varied up to 20-fold for the alga (72-h EC10 from 27.3 to 563 microg Zn/L), and approximately sixfold for the crustacean (21-d EC10 from 59.2 to 387 microg Zn/L), and fivefold for the fish (30-d LC10, lethal concentration for 10% of the organisms, from 185 to 902 microg Zn/L). For P. subcapitata a refined bioavailability model was developed by linking an empirical equation, which predicts toxicity expressed as free Zn2+ activity as a function of pH, to the geochemical speciation model WHAM/Model V. This model and previously developed acute and/or chronic biotic ligand models for D. magna and 0. mykiss generally predicted most effect concentrations by an error of less than a factor of two. In waters with pH > 8, however, chronic toxicity to D. magna was underestimated by a factor 3 to 4. Based on the results of this validation exercise and earlier research, we determined applicability ranges for pH (6-8) and Ca (5-160 mg/L) in which all three developed models are valid. Within these ranges, all three models may be considered useful tools for taking into account bioavailability in regulatory assessments of zinc.

Antioxidative Effect of Vitamin D3 on Zinc-Induced Oxidative Stress in CNS

Abstract: Antioxidative mechanisms of vitamin D3 were evaluated both in vitro and in vivo. A 4-h incubation of brain homogenates at 37 degrees C increased the formation of Schiff base fluorescent products of malonaldehyde, an indicator of lipid peroxidation. Incubation with vitamin D3 dose-dependently suppressed auto-oxidation. The antioxidative potency for inhibiting zinc-induced lipid peroxidation was as follows: vitamin D3 > Trolox (a water-soluble analogue of vitamin E) > or = beta-estradiol > melatonin. In the presence of high dose of desferrioxamine, a metal chelator, vitamin D3 attenuated auto-oxidation. These in vitro data indicate that vitamin D3 may act as a terminator of the lipid peroxidation chain reaction. The antioxidative effect of vitamin D3 on zinc-induced oxidative injury was verified using local infusion of vitamin D3 in vivo. Intranigral infusion of zinc elevated lipid peroxidation in the infused substantia nigra and depleted striatal dopamine content at 7 days after infusion. Furthermore, elevated cytosolic cytochrome c and DNA ladder, indicatives of apoptosis, were demonstrated in the infused substantia nigra. Simultaneous infusion of vitamin D3 and zinc prevented oxidative injury and apoptosis induced by zinc alone. The involvement of glia-derived neurotrophic factor (GDNF) expression was excluded since vitamin D3 did not alter GDNF level in the infused substantia nigra at 24 h or 4 days after intranigral infusion of vitamin D3. Our results suggest that vitamin D3, independent of upregulation of GDNF expression, may acutely prevent zinc-induced oxidative injuries via antioxidative mechanisms.