Showing papers on "Zinc toxicity published in 2013"

Heavy metal cu, ni and zn: toxicity, health hazards and their removaltechniques by low cost adsorbents: a short overview

Abstract: Electroplating and metalworking industries discharge large amounts of heavy metals, including copper (Cu), nickel (Ni) and zinc (Zn) ions, in their effluents have been recognized as a major problem to human health and aquatic life. Copper is highly toxic because it is non biodegradable and carcinogenic, Copper has been reported to cause neurotoxicity commonly known as “Wilson’s disease” due to deposition of copper in the lenticular nucleus of the brain and kidney failure, Nickel exposure vary from skin irritation to damage of the lungs, nervous system, and mucous membranes and Zinc toxicity from excessive ingestion is uncommon but causes gastrointestinal distress and diarrhea. The current regulation of waste water and drinking water standards are require contamination of heavy metal reduced up to few parts per million. Several processing techniques are available to reduce the concentrations of heavy metals in wastewater, including precipitation, flotation, ion exchange, solvent extraction, adsorption, cementation onto iron, membrane processing, and electrolytic methods. Adsorption onto activated carbon is a well-known method for removing toxic metal ions, but the high cost of activated carbon restricts its use in developing countries, so cheap and effective alternatives for the removal of heavy metals should reduce operating costs, reduce the prices of products, improve competitiveness, and benefit the environment. The adsorption abilities of a number of low-cost adsorbents (e.g., cheap zeolites, clay, coal fly ash, sewage sludge, agriculture waste, tea waste, rice husk, coconut husk, neem leaves and biomass) have been determined for the removal of heavy metals from water

High dose zinc supplementation induces hippocampal zinc deficiency and memory impairment with inhibition of BDNF signaling.

Abstract: Zinc ions highly concentrate in hippocampus and play a key role in modulating spatial learning and memory. At a time when dietary fortification and supplementation of zinc have increased the zinc consuming level especially in the youth, the toxicity of zinc overdose on brain function was underestimated. In the present study, weaning ICR mice were given water supplemented with 15 ppm Zn (low dose), 60 ppm Zn (high dose) or normal lab water for 3 months, the behavior and brain zinc homeostasis were tested. Mice fed high dose of zinc showed hippocampus-dependent memory impairment. Unexpectedly, zinc deficiency, but not zinc overload was observed in hippocampus, especially in the mossy fiber-CA3 pyramid synapse. The expression levels of learning and memory related receptors and synaptic proteins such as NMDA-NR2A, NR2B, AMPA-GluR1, PSD-93 and PSD-95 were significantly decreased in hippocampus, with significant loss of dendritic spines. In keeping with these findings, high dose intake of zinc resulted in decreased hippocampal BDNF level and TrkB neurotrophic signaling. At last, increasing the brain zinc level directly by brain zinc injection induced BDNF expression, which was reversed by zinc chelating in vivo. These results indicate that zinc plays an important role in hippocampus-dependent learning and memory and BDNF expression, high dose supplementation of zinc induces specific zinc deficiency in hippocampus, which further impair learning and memory due to decreased availability of synaptic zinc and BDNF deficit.

The BaeSR regulon is involved in defense against zinc toxicity in E. coli.

Abstract: Intracellular zinc homeostasis is regulated by an extensive network of transporters, ligands and transcription factors. The zinc detoxification functions of three transporters and a periplasmic protein regulated by the BaeSR two-component system were explored in this work by evaluating the effect of single gene knockouts in the BaeSR regulon on the cell growth rate, free zinc, total zinc and total copper after zinc shock. Two exporters, MdtABC and MdtD, and the periplasmic protein, Spy, are involved in zinc detoxification based on the growth defects at high cell density and increases in free (>1000-fold) and total zinc/copper (>2-fold) that were observed in the single knockout strains upon exposure to zinc. These proteins complement the ATP-driven zinc export mediated by ZntA in E. coli to limit zinc toxicity. These results highlight the functions of the BaeSR regulon in metal homeostasis.

The zinc transporter Zip5 (Slc39a5) regulates intestinal zinc excretion and protects the pancreas against zinc toxicity.

Abstract: Background ZIP5 localizes to the baso-lateral membranes of intestinal enterocytes and pancreatic acinar cells and is internalized and degraded coordinately in these cell-types during periods of dietary zinc deficiency. These cell-types are thought to control zinc excretion from the body. The baso-lateral localization and zinc-regulation of ZIP5 in these cells are unique among the 14 members of the Slc39a family and suggest that ZIP5 plays a role in zinc excretion. Methods/Principal Findings We created mice with floxed Zip5 genes and deleted this gene in the entire mouse or specifically in enterocytes or acinar cells and then examined the effects on zinc homeostasis. We found that ZIP5 is not essential for growth and viability but total knockout of ZIP5 led to increased zinc in the liver in mice fed a zinc-adequate (ZnA) diet but impaired accumulation of pancreatic zinc in mice fed a zinc-excess (ZnE) diet. Loss-of-function of enterocyte ZIP5, in contrast, led to increased pancreatic zinc in mice fed a ZnA diet and increased abundance of intestinal Zip4 mRNA. Finally, loss-of-function of acinar cell ZIP5 modestly reduced pancreatic zinc in mice fed a ZnA diet but did not impair zinc uptake as measured by the rapid accumulation of 67zinc. Retention of pancreatic 67zinc was impaired in these mice but the absence of pancreatic ZIP5 sensitized them to zinc-induced pancreatitis and exacerbated the formation of large cytoplasmic vacuoles containing secretory protein in acinar cells. Conclusions These studies demonstrate that ZIP5 participates in the control of zinc excretion in mice. Specifically, they reveal a paramount function of intestinal ZIP5 in zinc excretion but suggest a role for pancreatic ZIP5 in zinc accumulation/retention in acinar cells. ZIP5 functions in acinar cells to protect against zinc-induced acute pancreatitis and attenuate the process of zymophagy. This suggests that it may play a role in autophagy.

Synergistic Effects of Nano-Sized Titanium Dioxide and Zinc on the Photosynthetic Capacity and Survival of Anabaena sp.

Abstract: Anabaena sp. was used to examine the toxicity of exposure to a nano-TiO2 suspension, Zn2+ solution, and mixtures of nano-TiO2 and Zn2+ suspensions. Typical chlorophyll fluorescence parameters, including effective quantum yield, photosynthetic efficiency and maximal electron transport rate, were measured by a pulse-amplitude modulated fluorometer. Nano-TiO2 particles exhibited no significant toxicity at concentrations lower than 10.0 mg/L. The 96 h concentration for the 50% maximal effect (EC50) of Zn2+ alone to Anabaena sp. was 0.38 ± 0.004 mg/L. The presence of nano-TiO2 at low concentrations (<1.0 mg/L) significantly enhanced the toxicity of Zn2+ and consequently reduced the EC50 value to 0.29 ± 0.003 mg/L. However, the toxicity of the Zn2+/TiO2 system decreased with increasing nano-TiO2 concentration because of the substantial adsorption of Zn2+ by nano-TiO2. The toxicity curve of the Zn2+/TiO2 system as a function of incremental nano-TiO2 concentrations was parabolic. The toxicity significantly increased at the initial stage, reached its maximum, and then decreased with increasing nano-TiO2 concentration. Hydrodynamic sizes, concentration of nano-TiO2 and Zn2+ loaded nano-TiO2 were the main parameters for synergistic toxicity.

Changes in growth and biochemical status of common carp, Cyprinus carpio L. exposed to water-born zinc toxicity for different periods

Abstract: The present study was carried out to investigate the effect of sublethal zinc (Zn) concentrations on the growth, biochemical variables, and Zn residues in common carp, Cyprinus carpio L.. Fish (18.1 – 19.1 g) were exposed to 0.0 (control), 5.0 and 10.0 mg Zn/L for 7, 14, 28, and 56 days. At each time interval and each treatment, fish were collected, weighed and sampled to measure the growth, biochemical variables, and Zn residues in whole-fish body. Growth performance was significantly reduced with increasing Zn concentrations. However, fish exposed to 10.0 mg Zn/L for 56 days grew lower than that of the control group. Likewise, the optimum feed intake and feed conversion ratio were obtained at control group at 56 days. Furthermore, glucose, AST, ALT, creatinine, and cortisol increased significantly with increasing Zn concentration and exposure time, with maximal values at 56 days. Meanwhile, the highest values of serum protein and lipids of were obtained in the control fish reared for 56 days, whereas the lowest values were observed in fish exposed to 10.0 mg Zn/L for 56 days. The content of whole-body moisture and total ash increased significantly, while crude protein and total lipid contents decreased significantly with increasing Zn concentrations. In addition, Zn exposure increased Zn residues in fish body; however, Zn bioaccumulation in fish body was Zn dose and time dependant. The present study revealed that the growth and health status of common carp were deteriorated by Zn toxicity.

Cobalt chloride speciation, mechanisms of cytotoxicity on human pulmonary cells, and synergistic toxicity with zinc

Abstract: Cobalt is used in numerous industrial sectors, leading to occupational diseases, particularly by inhalation. Cobalt-associated mechanisms of toxicity are far from being understood and information that could improve knowledge in this area is required. We investigated the impact of a soluble cobalt compound, CoCl2·6H2O, on the BEAS-2B lung epithelial cell line, as well as its impact on metal homeostasis. Cobalt speciation in different culture media, in particular soluble and precipitated cobalt species, was investigated via theoretical and analytical approaches. The cytotoxic effects of cobalt on the cells were assessed. Upon exposure of BEAS-2B cells to cobalt, intracellular accumulation of cobalt and zinc was demonstrated using direct in situ microchemical analysis based on ion micro-beam techniques and analysis after cell lysis by inductively coupled plasma mass spectrometry (ICP-MS). Microchemical imaging revealed that cobalt was rather homogeneously distributed in the nucleus and in the cytoplasm whereas zinc was more abundant in the nucleus. The modulation of zinc homeostasis led to the evaluation of the effect of combined cobalt and zinc exposure. In this case, a clear synergistic increase in toxicity was observed as well as a substantial increase in zinc content within cells. Western blots performed under the same coexposure conditions revealed a decrease in ZnT1 expression, suggesting that cobalt could inhibit zinc release through the modulation of ZnT1. Overall, this study highlights the potential hazard to lung function, of combined exposure to cobalt and zinc.

Zinc Toxicity in Tomato Plants

Abstract: Tomato (cultivar PKM -1) plants were raised in pots containing the soil amended with various levels of zinc (control, 50, 100, 150, 200 and 250 mg kg soil). Five replicates were maintained for each level. 1

In vivo zinc toxicity phenotypes provide a sensitized background that suggests zinc transport activities for most of the Drosophila Zip and ZnT genes.

Abstract: Members of the ZIP (SLC39A) and ZnT (SLC30A) families of transmembrane domain proteins are predicted to transport the essential transition metal zinc across membranes, regulating cellular zinc content and distribution via uptake and efflux at the outer plasma and organellar membranes. Twenty-four ZIP and ZnT proteins are encoded in mammalian genomes, raising questions of whether all actually transport zinc, whether several function together in the same tissues/cell types, and how the activity of these transporters is coordinated. To address these questions, we have taken advantage of the ability to manipulate several genes simultaneously in targeted cell types in Drosophila. Previously we reported zinc toxicity phenotypes caused by combining overexpression of a zinc uptake gene, dZip42C.1, with suppression of a zinc efflux gene, dZnT63C. Here we show that these phenotypes can be used as a sensitized in vivo system to detect subtle alterations in zinc transport activity that would be buffered in healthy cells. Using two adult tissues, the fly eye and midline (thorax/abdomen), we find that when overexpressed, most of the 17 DrosophilaZip and ZnT genes modify the zinc toxicity phenotypes in a manner consistent with their predicted zinc transport activity. In most cases, we can reconcile that activity with the cellular localization of an enhanced green fluorescent protein tagged version of the protein. Additionally, targeted suppression of each gene by RNA interference reveals several of the fly Zip and ZnT genes are required in the eye, indicating that numerous independent zinc transport genes are acting together in a single tissue.

Zinc toxicity on antioxidative response in (Zea mays L.) at two different pH

Abstract: Zn is the second most abundant transition metal after iron (Fe). Excess Zn can have negative effects on plants. The effect of Zn at two different pH on lipid peroxidation (MDA), membrane permeability (EC), hydrogen peroxide (H 2 O 2 ), non-protein thiols (NPT) and the activities of major antioxidant enzymes Zea mays were investigated under controlled growth conditions. Zn-excess conditions increased the EC, MDA, H 2 O 2 content and non-protein thiols and also activities of antioxidant enzymes were increased. Also zinc toxicity was higher in 4.5 pH than 7.5 pH.

Sublethal zinc and copper exposure affect acetylcholinesterase activity and accumulation in different tissues of Leporinus obtusidens.

Abstract: In this study, we investigated zinc and copper effects on acetylcholinesterase (AChE, EC. 3.1.1.7) activity and metal accumulation in tissues of native fish Leporinus obtusidens (piava). Fish were exposed to 10 and 20 % of the LC50 that corresponded at 2.28 and 4.57 mg/L (zinc) and 0.018 and 0.038 mg/L (copper) for 30 and 45 days. The AChE activity was evaluated in brain and white muscle of fish and metals accumulation was measured in kidney, liver, muscle and brain. Exposure to zinc and copper significantly increased AChE activity in both tissues and times tested, except for brain AChE activity at 2.28 mg/L of Zn (II) after 45 days where a reduction of 52.5 % was observed. Fish exposed to zinc showed accumulation of this metal in liver and kidney in both concentrations and times tested. A different result was obtained for copper: significant copper accumulation was obtained only in brain at both concentrations tested after 45 days of exposure. These results suggest that piavas exposed to zinc and copper showed changes in AChE activity and also demonstrate accumulation in some tissues. These results demonstrate that L. obtusidens could be a good bioindicator to evaluate water containing metals. The metal accumulation absence in muscle tissue is an indicative of low potential contamination by metals in this fish species.

Characterization of a Heavy Metal Translocating P-Type ATPase Gene from an Environmental Heavy Metal Resistance Enterobacter sp. Isolate

Abstract: Heavy metals are common contaminants found in polluted areas. We have identified a heavy metal translocating P-type ATPase gene (hmtp) via fosmid library and in vitro transposon mutagenesis from an Enterobacter sp. isolate. This gene is believed to participate in the bacterium’s heavy metal resistance traits. The complete gene was identified, cloned, and expressed in a suitable Escherichia coli host cell. E. coli W3110, RW3110 (zntA::Km), GG48 (ΔzitB::Cm zntA::Km), and GG51 (ΔzitB::Cm) were used to study the possible effects of this gene for heavy metal (cadmium and zinc in particular) resistance. Among the E. coli strains tested, RW3110 and GG48 showed more sensitivity to cadmium and zinc compared to the wild-type E. coli W3110 and strain GG51. Therefore, strains RW3110 and GG48 were chosen for the reference hosts for further evaluation of the gene’s effect. The results showed that expression of this heavy metal translocating P-type ATPase gene could increase the ability for zinc and cadmium resistance in the tested microorganisms.

Angiotensin II potentiates zinc-induced cortical neuronal death by acting on angiotensin II type 2 receptor

Abstract: The angiotensin system has several non-vascular functions in the central nervous system. For instance, inhibition of the brain angiotensin system results in a reduction in neuronal death following acute brain injury such as ischemia and intracerebral hemorrhage, even under conditions of constant blood pressure. Since endogenous zinc has been implicated as a key mediator of ischemic neuronal death, we investigated the possibility that the angiotensin system affects the outcome of zinc-triggered neuronal death in cortical cell cultures. Exposure of cortical cultures containing neurons and astrocytes to 300 μM zinc for 15 min induced submaximal death in both types of cells. Interestingly, addition of angiotensin II significantly enhanced the zinc-triggered neuronal death, while leaving astrocytic cell death relatively unchanged. Both type 1 and 2 angiotensin II receptors (AT1R and AT2R, respectively) were expressed in neurons as well as astrocytes. Zinc neurotoxicity was substantially attenuated by PD123319, a specific inhibitor of AT2R, and augmented by CGP42112, a selective activator of AT2R, indicating a critical role for this receptor subtype in the augmentation of neuronal cell death. Because zinc toxicity occurs largely through oxidative stress, the levels of superoxides in zinc-treated neurons were assessed by DCF fluorescence microscopy. Combined treatment with zinc and angiotensin II substantially increased the levels of superoxides in neurons compared to those induced by zinc alone. This increase in oxidative stress by angiotensin II was completely blocked by the addition of PD123319. Finally, since zinc-induced oxidative stress may be caused by induction and/or activation of NADPH oxidase, the activation status of Rac and the level of the NADPH oxidase subunit p67phox were measured. Angiotensin II markedly increased Rac activity and the levels of p67phox in zinc-treated neurons and astrocytes in a PD123319-dependent manner. The present study shows that the angiotensin system, especially that involving AT2R, may have an oxidative injury-potentiating effect via augmentation of the activity of NADPH oxidase. Hence, blockade of angiotensin signaling cascades in the brain may prove useful in protecting against the oxidative neuronal death that is likely to occur in acute brain injury.