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.

Acute zinc toxicity to Cnesterodon decemmaculatus (Pisces: Poeciliidae) and application of the Biotic Ligand Model in Pilcomayo River water (South America)

Abstract: The Biotic Ligand Model (BLM) is a chemical equilibrium-based model that incorporates the effect of physicochemical water characteristics on the bioavailability and toxicity of metals to aquatic biota. It was developed for four metals (Cu, Zn, Ag and Cd), two fish species and three daphnids. It is assumed that its predictions can be extrapolated between similar species. In this study, a cross-fish-species extrapolation of the BLM developed for zinc (Zn-BLM) was assessed in Pilcomayo River water. An acute zinc toxicity test was performed to assess zinc toxicity to the local fish Cnesterodon decemmaculatus. The dissolved -1 zinc concentrations tested were: 3.74; 9.2; 21.6 and 26.4 mg Zn L. The median letal zinc concentration (96-h Zn LC ) calculated for C. 50 -1 decemmaculatus was 22.6 mg Zn L (17.5-27.6) and the predicted by −1 Zn-BLM for Pimephales promelas in the test water was 1.71 mg L. Zinc concentrations measured exceeded zinc solubility causing metal precipitation which derived in a 96-h LC that most probably 50 included both dissolved and precipitated zinc species. Nevertheless, speciation estimates showed that the more abundant zinc species in each treatment was the free ion. This higher proportion of zinc in its free ionic form would explain the low protective effect exerted by elevated water hardness. The difference between the observed zinc toxicity to C. decemmaculatus and the predicted by BLM for P. promelas may be due to the combination of inaccuracy in zinc dissolved measurements and a lower sensitivity of C. decemmaculatus to zinc exposure.

Effect of phosphorus on zinc toxicity in tea pollen tube growth

Abstract: Although zinc (Zn) is an essential element for the growth of higher plants, excess supply may lead to growth inhibition. Symptoms of Zn toxicity are characterized by a reduction in root growth and leaf expansion followed by chlorosis (Mengel and Kirkby 1987), especially root elongation is severely inhibited (Godbold et al. 1983). Due to the increase of input of Zn to farmland by the application of sewage sludge or large amounts of Zn-containing pig manure, Zn toxicity may become an important problem in certain regions (Ruano et al. 1987). In addition, Zn toxicity is also a problem in some acidic soils (Takahashi et al. 1980). Increasing soil pH by liming is the most effective procedure for decreasing both Zn content and Zn toxicity in plants (White et al. 1979), because Zn solubility decreases 100 times for each unit increase in pH (Neue and Lantin 1994). As an alternative approach, application of large amounts of phosphorus (P) fertilizer was employed to detoxify Zn (Takahashi et al. 1980). Howe...

Effect of Zinc and DHA on Expression Levels and Post-Translational Modifications of Histones H3 and H4 in Human Neuronal Cells

Abstract: Docosahexaenoic acid (DHA) is an important omega-3 fatty acid required for the development of the human central nervous system and the continuous maintenance of neuronal cell function. The DHA composition of the brain decreases with age possibly as a result of increased oxidative damage to the lipid membranes (Schaefer, Bongard et al. 2006). Epidemiological studies have shown that patients with Alzheimer's disease (AD) have significantly lower levels of omega-3 fatty acids in their plasma phospholipids (Moriguchi, Greiner et al. 2000; Friedland 2003). There is an association between DHA levels in the brain and zinc homeostasis, which is particularly interesting as both are involved in neuroprotection. A reduction of DHA levels in the brain causes over expression of ZnT3, a transmembrane proteins that is associated with sequestration of cytoplasmic Zn2+ into synaptic vesicles (Jayasooriya, Ackland et al. 2005), resulting in zinc toxicity and neuronal cell death in cultured neuronal cells (Suphioglu, De Mel et al. 2010a; Naganska and Matyja 2006). Mice that lacked a zinctransporting gene ZnT3 were shown to develop fewer and smaller plaques than Alzheimer's-prone mice with the gene (Lee, Cole et al. 2002), suggesting that altered zinc homeostasis may contribute to the plaque formation in AD. DHA, on the other hand, has neuroprotective properties against neurodegenerative diseases. Dietary supplement of omega-3 fatty acid may protect against Alzheimer’s disease, through inhibiting amyloid plague formation (Calon, Lim et al. 2004; Oksman, Iivonen et al. 2006; Florent-Bechard, Malaplate-Armand et al. 2007). DHA was also observed to significantly increase neuronal survival by preventing cytoskeleton perturbations, caspase activation and apoptosis (Florent-Bechard, Malaplate-Armand et al. 2007). Our recent data has shown that histone gene and protein expression were affected by both zinc and DHA. The expression levels of histones H3 and H4, in human neuronal cells, were down-regulated by zinc and up-regulated by DHA (Suphioglu, Sadli et al. 2010b), suggesting a possible interaction between the two nutrients. Further investigations into the

PROTECTIVE EFFECT OF Se AGAINST Zn TOXICITY ON ULTRASTRUTURE OF PAVLOVA VIRIDIS TSENG (HAPTOPHYCEAE)

Abstract: The protective effects of selenium against zinc toxicity in the flagellate alga Pavlova viridis were investigated using transmission electron microscopy. Cells from a control and two experimental groups were compared for their ultrastructural characteristics. In experimental group one, the culture medium was treated with 15 mg L -1 Zn (ZnSO 4·7H 2O), while in group two, it with both 15 mg L -1 Se (Na 2SeO 3·5H 2O) and 15 mg L -1Zn. The results showed that the independent use of Zn at a concentration of 15 mg L -1 caused serious damage to the chloroplast tetrolobes in the algae, yet this effect was prevented in the presence of Se. The algal cells affected by Zn had variously-sized, electron-dense bodies in cytoplasm and chloroplast matrix. In contrast, the cells treated with both Zn and Se were characterized by the occurrence of electron-dense particles in vacuole inclusion body. Accordingly, the following hypothesis was made: when acting alone, the extra Zn in P. viridis cells was compartmented in particular molecules, identified as electron-dense bodies, whereas this process was inhibited by the formation of Zn selenides, in which the Zn was inactivated, thereby protecting the cells against Zn toxicity. Fig 3, Tab 1, Ref 28