Showing papers on "Zinc toxicity published in 2009"
TL;DR: It is suggested that excess Zn exerts its toxicity partially through disturbing nutrient balance and inducing oxidative stress in plants through the adaptive mechanism in Zn non-hyperaccumulator plants.
234 citations
TL;DR: TRPA1 is identified as an important target for the sensory effects of zinc and an emerging role for zinc as a signaling molecule that can modulate sensory transmission is supported, as low nanomolar concentrations activate TRPA1 and modulate its sensitivity.
Abstract: Zinc is an essential biological trace element. It is required for the structure or function of over 300 proteins, and it is increasingly recognized for its role in cell signaling. However, high concentrations of zinc have cytotoxic effects, and overexposure to zinc can cause pain and inflammation through unknown mechanisms. Here we show that zinc excites nociceptive somatosensory neurons and causes nociception in mice through TRPA1, a cation channel previously shown to mediate the pungency of wasabi and cinnamon through cysteine modification. Zinc activates TRPA1 through a unique mechanism that requires zinc influx through TRPA1 channels and subsequent activation via specific intracellular cysteine and histidine residues. TRPA1 is highly sensitive to intracellular zinc, as low nanomolar concentrations activate TRPA1 and modulate its sensitivity. These findings identify TRPA1 as an important target for the sensory effects of zinc and support an emerging role for zinc as a signaling molecule that can modulate sensory transmission.
203 citations
TL;DR: A more than additive effect was indicated by the acute tests for both species exposed toCu+Pb, for D. carinata exposed to Cu+Zn, and for C. dubia exposed to all three metals.
139 citations
TL;DR: The role of zinc in health and disease has been studied through patients with toxicity or severe deficiency with obvious clinical signs, but the prevalence of zinc deficiency and its contribution to disease in veterinary patients is not well known.
Abstract: Objective – To review zinc physiology and pathophysiology and the importance of zinc toxicity and deficiency in veterinary patients.
Data Sources – A review of human and veterinary medical literature.
Human Data Synthesis – There is a significant amount of original research in humans and animals on the role of zinc in multiple organ systems. There is also significant data available on human patients with zinc abnormalities.
Veterinary Data Synthesis – Zinc deficiency has been studied in dogs with genetic disease and dietary deficiency leading to dermatological disease and immune deficiency. Zinc toxicity has been described after ingestion of metallic foreign bodies containing zinc.
Conclusions – Historically, the role of zinc in health and disease has been studied through patients with toxicity or severe deficiency with obvious clinical signs. As the ubiquitous contribution of zinc to structure and function in biological systems was discovered, clinically significant but subtle deficiency states have been revealed. In human medicine, mild zinc deficiencies are currently thought to cause chronic metabolic derangement leading to or exacerbating immune deficiency, gastrointestinal problems, endocrine disorders, neurologic dysfunction, cancer, accelerated aging, degenerative disease, and more. Determining the causal relationships between mild zinc deficiency and concurrent disease is complicated by the lack of sensitive or specific tests for zinc deficiency. The prevalence of zinc deficiency and its contribution to disease in veterinary patients is not well known. Continued research is warranted to develop more sensitive and specific tests to assess zinc status, to determine which patients are at risk for deficiency, and to optimize supplementation in health and disease.
98 citations
TL;DR: Tolerance to photo-oxidative stress induced by paraquat was another distinctive feature of the MAT-PsMTA1 lines, and low levels of DNA damage were detected by quantifying the amounts of 8-hydroxy-2′-deoxyguanosine in leaf tissues of the transgenic plants exposed to copper.
Abstract: Marker-free transgenic white poplar (Populus alba L., cv 'Villafranca') plants, expressing the PsMT (A1) gene from Pisum sativum for a metallothionein-like protein, were produced by Agrobacterium tumefaciens-mediated transformation. The 35SCaMV-PsMT (A1)-NosT cassette was inserted into the ipt-type vector pMAT22. The occurrence of the abnormal ipt-shooty phenotype allowed the visual selection of transformants, while the yeast site-specific recombination R/RS system was responsible for the excision of the undesired vector sequences with the consequent recovery of normal marker-free transgenic plants. Molecular analyses confirmed the presence of the 35SCaMV-PsMT (A1)-NosT cassette and transgene expression. Five selected lines were further characterized, revealing the ability to withstand heavy metal toxicity. They survived 0.1 mM CuCl(2), a concentration which strongly affected the nontransgenic plants. Moreover, root development was only slightly affected by the ectopic expression of the transgene. Reactive oxygen species were accumulated to a lower extent in leaf tissues of multi-auto-transformation (MAT)-PsMT(A1) plants exposed to copper and zinc, compared to control plants. Tolerance to photo-oxidative stress induced by paraquat was another distinctive feature of the MAT-PsMT(A1) lines. Finally, low levels of DNA damage were detected by quantifying the amounts of 8-hydroxy-2'-deoxyguanosine in leaf tissues of the transgenic plants exposed to copper.
79 citations
TL;DR: It is indicated that cadmium, lead and zinc can induce micronucleated cells, SCEs and sperm abnormalities in Algerian mice and that the clastogenic potential is dependent on the time of exposure and the interaction between the three elements, confirming the environmental damage that may result from the simultaneous action of several metals.
Abstract: As a consequence of human activities, large amounts of cadmium, lead and zinc are released in the environment, often simultaneously. The aim of this study was to investigate under experimental conditions the DNA damage induced in Algerian mice (Mus spretus) exposed to cadmium (Cd), lead (Pb) and zinc (Zn) separately, or in selected combinations. Three cytogenetic end points were considered: the frequencies of micronucleated cells (MN) and sister chromatid exchange (SCE) in the bone marrow and the frequency of sperm abnormalities. Mice were treated by intraperitoneal (i.p.) injections with 5 or 10 doses of aqueous solutions of cadmium acetate, lead acetate and zinc acetate in concentrations corresponding to 1/10 of the LD50, respectively, 21.5, 0.46 and 1.5 mg/kg bw. The control groups were injected in the same way with distilled water. With only one exception (Cd + Zn group treated with 5 doses), the results show a significant increase of MN in all groups for both treatments (5 and 10 doses). Similarly, the results concerning the SCE revealed a statistically significant increase in all treated animals, with the exception of the Zn group treated with 5 doses. The number of sperm abnormalities was significantly higher in animals treated with 5 doses, except in the group Pb + Zn. In animals treated with 10 doses the number of sperm abnormalities was always statistically higher compared with controls. This study indicates that cadmium, lead and zinc can induce MN, SCEs and sperm abnormalities in Algerian mice and that the clastogenic potential is dependent on the time of exposure and the interaction between the three elements, confirming the environmental damage that may result from the simultaneous action of several metals. Most relevant is the toxic potential for Zn, related with the dose, which may compromise its protective effect against other metal contaminations, such as cadmium.
61 citations
TL;DR: This study describes the growth inhibition of C. vulgaris exposed to different concentrations of cadmium and zinc, and the induction of metal-binding MT-like proteins in the cells, and suggests that these proteins might be involved in the detoxification of heavy metals by the alga.
59 citations
TL;DR: Results indicate that covalent tyrosine dimerization of a SLC30A family member modulates its subcellular localization and zinc transport capacity and propose that dityrosine-dependent membrane protein oligomerization may regulate the function of diverse membrane protein in normal and disease states.
Abstract: Non-covalent and covalent homo-oligomerization of membrane proteins regulates their subcellular localization and function Here, we described a novel oligomerization mechanism affecting solute carrier family 30 member 3/zinc transporter 3 (SLC30A3/ZnT3) Oligomerization was mediated by intermolecular covalent dityrosine bonds Using mutagenized ZnT3 expressed in PC12 cells, we identified two critical tyrosine residues necessary for dityrosine-mediated ZnT3 oligomerization ZnT3 carrying the Y372F mutation prevented ZnT3 oligomerization, decreased ZnT3 targeting to synaptic-like microvesicles (SLMVs), and decreased resistance to zinc toxicity Strikingly, ZnT3 harboring the Y357F mutation behaved as a “gain-of-function” mutant as it displayed increased ZnT3 oligomerization, targeting to SLMVs, and increased resistance to zinc toxicity Single and double tyrosine ZnT3 mutants indicate that the predominant dimeric species is formed between tyrosine 357 and 372 ZnT3 tyrosine dimerization was detected under normal conditions and it was enhanced by oxidative stress Covalent species were also detected in other SLC30A zinc transporters localized in different subcellular compartments These results indicate that covalent tyrosine dimerization of a SLC30A family member modulates its subcellular localization and zinc transport capacity We propose that dityrosine-dependent membrane protein oligomerization may regulate the function of diverse membrane protein in normal and disease states
54 citations
TL;DR: The main purpose of the present study was to detect the acute toxicity of cadmium and zinc to F. paulensis and investigate their effects on oxygen consumption and ammonium excretion, investigations that have not been carried out in this species before.
Abstract: In Brazil, pink shrimp (Farfantepenaeus paulensis) is an important commercially exploited species and is an ideal animal for studying the impairment caused by the effects of heavy metals that are often detected in coastal areas. The main purpose of the present study was to detect the acute toxicity of cadmium and zinc to F. paulensis and investigate their effects on oxygen consumption and ammonium excretion, investigations that have not been carried out in this species before. First, the acute toxicity of zinc and cadmium to F. paulensis for 24, 48, 72, and 96 h--medium lethal concentration was examined, which resulted in the following values: 9.39, 6.00, 4.88, and 3.31 mg/l for zinc and 2.35, 1.67, 1.26, and 0.83 mg/l for cadmium. Furthermore, we also found that exposure of shrimp to zinc and cadmium caused an inhibition in oxygen consumption of 25 and 32.4%, respectively, relative to the control. In addition, after separate exposure to cadmium and zinc, elevations in ammonium excretion were obtained, which were 42.85 and 51.85% higher than the control, respectively.
45 citations
TL;DR: The results from these experiments indicate that zinc contamination of streams can have sublethal effects on populations and physiology of fish that are able to survive in the contaminated water.
Abstract: A section of the Upper Enoree River in South Carolina, USA, was contaminated with chemical waste in 1985, and high concentrations of zinc persist decades later. In this study, we examined the zinc concentrations in the water, the accumulation of zinc in a variety of fish tissues, the effects of the contaminated water on fish sperm motility in vitro, and the mortality rates of introduced fish. Zinc concentrations in the water samples collected from six sites decreased as distance from the spill site increased, ranging from 7.3 to 0.34 mg/L (p < 0.001). The zinc concentrations of tissues from native fish were highest in liver (mean across sites of 110 ppm/g tissue) and gills (77.4 ppm/g tissue), followed by gonads (30.7 ppm/g tissue) and muscle (6.9 ppm/g tissue) (p < 0.001). The duration of fast motility of Salmo trutta sperm was significantly diminished in sperm activated in samples from the contaminated stream compared with the control stream (p < 0.05). To further evaluate the ability of fish to survive at the sites with different zinc concentrations, groups of Gambusia holbrooki were placed in traps at a reference site (uncontaminated local tributary), and three sites along the contaminated stream. Rapid mortality was observed in the two sites closest to the spill, including one site in which native fish had been found. The introduced G. holbrooki expressed higher zinc concentration in gills than gonads or muscle (p < 0.001), and water zinc concentration significantly affected fish mortality (p < 0.001). The results from these experiments indicate that zinc contamination of streams can have sublethal effects on populations and physiology of fish that are able to survive in the contaminated water.
42 citations
TL;DR: It is shown that iron starvation affects zinc metabolism by downregulating expression of the plasma membrane zinc importer encoding zrfB and upregulating the putative vacuolar zinc transporter-encoding zrcA in Aspergillus fumigatus, demonstrating a fine tuned coordination of zinc and iron metabolism in A. fmigatus.
TL;DR: The strong ability of these cyanobacteria to acclimate to different environments is suggested, indicating that M. aeruginosa become very sensitive to metals following 1-day recovery, consistent with the significant increase in metal uptake.
TL;DR: It is concluded that clay content had no significant influence on sub-lethal toxicity of zinc to this earthworm over the range of exposure concentrations.
TL;DR: The hazard index of arsenic, zinc, and copper mixture for intake of milkfish demonstrated that intake of in this way contaminated milkfish will result in non-carcinogenic risk.
Abstract: Studies on bioaccumulation of arsenic, zinc, and copper in freshwater-cultured milkfish were carried out to assess the risks on human health. The arsenic, zinc, and copper levels in milkfish showed significant positive correlations to the arsenic, zinc, and copper concentrations in pond water. The hazard index of arsenic, zinc, and copper mixture for intake of milkfish (1.75 +/- 0.65) demonstrated that intake of in this way contaminated milkfish will result in non-carcinogenic risk. The target cancer risk of arsenic for intake of the milkfish (2.74 x 10(-4) +/- 1.18 x 10(-4)) indicated that the inhabitants were exposed to arsenic pollution with carcinogenic risk.
TL;DR: Exposure to zinc increases iron uptake by respiratory epithelial cells and it is concluded that changes in iron homeostasis may contribute to the biological effects of zinc in specific cells and tissues.
Abstract: Despite recurrent exposure to zinc through inhalation of ambient air pollution particles, relatively little information is known about the homeostasis of this metal in respiratory epithelial cells. We describe zinc uptake and release by respiratory epithelial cells and test the postulate that Zn(2+) transport interacts with iron homeostasis in these same cells. Zn(2+) uptake after 4 and 8 h of exposure to zinc sulfate was concentration- and time-dependent. A majority of Zn(2+) release occurred in the 4 h immediately following cell exposure to ZnSO(4). Regarding metal importers, mRNA for Zip1 and Zip2 showed no change after respiratory epithelial cell exposure to zinc while mRNA for divalent metal transporter (DMT)1 increased. Western blot assay for DMT1 protein supported an elevated expression of this transport protein following zinc exposure. RT-PCR confirmed mRNA for the metal exporters ZnT1 and ZnT4 with the former increasing after ZnSO(4). Cell concentrations of ferritin increased with zinc exposure while oxidative stress, measured as lipid peroxides, was decreased supporting an anti-oxidant function for Zn(2+). Increased DMT1 expression, following pre-incubations of respiratory epithelial cells with TNF-alpha, IFN-gamma, and endotoxin, was associated with significantly decreased intracellular zinc transport. Finally, incubations of respiratory epithelial cells with both zinc sulfate and ferric ammonium citrate resulted in elevated intracellular concentrations of both metals. We conclude that exposure to zinc increases iron uptake by respiratory epithelial cells. Elevations in cell iron can possibly affect an increased expression of DMT1 and ferritin which function to diminish oxidative stress. Comparable to other metal exposures, changes in iron homeostasis may contribute to the biological effects of zinc in specific cells and tissues.
TL;DR: In this article, the authors evaluated acute and subchronic toxicity of arsenite (As(3+)) and zinc (Zn(2+)) to stage 25 tadpoles of Rhinella arenarum in both single and joint laboratory exposures.
Abstract: The current study evaluated acute and subchronic toxicity of arsenite (As(3+)) and zinc (Zn(2+)) to stage 25 tadpoles of Rhinella arenarum in both single and joint laboratory exposures. LC50 values obtained for As(3+) were elevated and remained within the range of 46 to 50 mg/L of As(3+) between 4 and 17 d of exposure. Growth of tadpoles was completely inhibited with 30 mg/L of As(3+), demonstrating the presence of ecologically relevant sublethal effects at concentrations lower than those resulting in lethality. With respect to Zn(2+), a 96-h LC50 value of 2.49 mg/L was calculated in soft water. Contrary to results obtained for As(3+), LC50 values of Zn(2+) gradually decreased with increasing exposure duration, from 2.49 mg/L at 96 h to 1.30 mg/L after 21 d. In joint exposures to both metals, the type of interaction observed between As(3+) and Zn(2+) was concentration dependent. Lethal effects of As(3+) were mitigated, unaffected, or potentiated by 0.01, 0.1, and 1-2 mg/L of Zn(2+), respectively. However, although 0.01 mg/L of Zn(2+) significantly reduced lethality of As(3+)-exposed tadpoles, the same concentration of Zn(2+) did not help to reverse the stunt growth of these animals. Further studies need to examine which are the lowest concentrations As(3+) required to reduce growth and whether Zn(2+) serves to antagonize growth effects in this range of concentrations.
TL;DR: It was found that an elevated cellular P concentration significantly promoted the short‐term uptake of Cd and Zn by M. aeruginosa and the P‐replete cells were more tolerant of [Cd2+]or[Zn2+]; but became more sensitive to Cd toxicity when incubated in a P‐deficient medium.
Abstract: In the present study, we quantified the 4-h uptake and 48-h toxicity of Cd and Zn in a freshwater cyanobacterium, Microcystis aeruginosa, under varied cellular and ambient P concentrations. After acclimation under different P conditions, the cyanobacteria had different cellular P concentrations. We found that an elevated cellular P concentration significantly promoted the short-term uptake of Cd and Zn by M. aeruginosa. With an increase in the cellular P concentration from 66 to 118 micromol/g, the uptake rates of Cd and Zn increased by 40- and 16-fold, respectively, and a significant exponential relationship between metal uptake rate and cellular P concentration was observed. The pulse amplitude-modulated parameter (maximum photosystem II quantum yield) and cell-specific growth rate were used as toxicity endpoints of cyanobacteria over 48 h of metal exposure. The P-replete cells were more tolerant of [Cd2+] or [Zn2+] than the P-starved cells but became more sensitive to Cd toxicity when incubated in a P-deficient medium. The polyphosphate bodies may have formed in the cyanobacterial cells under surplus P conditions, which can serve as a metal sink to sequester/detoxify the incoming Cd and Zn. The geometric means of median inhibition concentration based on the cellular metal to P ratio (mol:mol) were 0.041 and 0.036 for Cd and Zn, respectively. The cellular metal to P ratio was better than the cellular P concentration at predicting the toxic effects of metals under different P conditions.
TL;DR: New evidence suggests that activation of the irritant receptor, TRPA1, which is expressed on pain-sensing neurons, may be responsible for some of these symptoms of zinc toxicity.
Abstract: Exposure to zinc can cause pain and inflammation and can be harmful to human health. New evidence suggests that activation of the irritant receptor, TRPA1, which is expressed on pain-sensing neurons, may be responsible for some of these symptoms of zinc toxicity.
TL;DR: Cd-induced adaptive and cross-protective responses against Cd and Zn toxicity are the important mechanisms used by Ralstonia sp.TAK1 to survive in the heavy metal contaminated environments.
01 Jan 2009
TL;DR: Toxicity of zinc to Pseudomonas, Escherichia, Proteus, Bacillus and Arthrobacter species isolated from a tropical river and petroleum refinery effluent was assessed using TTCdehydrogenase activity (DHA) inhibition test.
Abstract: Toxicity of zinc to Pseudomonas , Escherichia , Proteus , Bacillus and Arthrobacter species isolated from a tropical river and petroleum refinery effluent was assessed using TTCdehydrogenase activity (DHA) inhibition test. At sufficient concentrations, zinc is toxic to these bacterial cells, and the exposure of the cells to zinc ion resulted in repression of dehydrogenase activity. The patterns of these toxic effects can be mathematically described with logistic dose-response models and in a manner similar to the non-competitive inhibition of enzymes. The threshold concentration above which toxic effect is observed ranged from 0.008 mM for Pseudomonas sp. DAF1 to 0.364 mM for Proteus sp. PLK2. The coefficients of inhibition Ki correlated with the IC 50 and indicate that zinc toxicity is dependent on the organism. The Ki and toxicity threshold values predicted from the equations are comparable and are suitable indicators for kinetic analyses of zinc toxicity against bacteria.