Showing papers on "Zinc toxicity published in 2003"

Effect of metal toxicity on plant growth and metabolism: I. Zinc

Abstract: Zinc toxicity and problems with regard to tolerance and ecological significance are briefly discussed. Differential tolerance of plant genotypes exposed to zinc toxicity is a promising approach to enrich our understanding of zinc tolerance in plants. Knowledge concerning the physiology and biochemistry with regard to phytotoxicity, uptake and transport of zinc and tolerance and its characterization are also discussed. The cytotoxic effects of zinc on plants are elucidated. The major change was seen in the nucleus of the root tip cells due to zinc toxicity. The chromatin material was highly condensed and some of the cortical cells showed disruption and dilation of nuclear membrane in presence of 7.5 mM zinc. The cytoplasm became structureless, disintegration of cell organelles and the development of vacuoles were also observed. The number of nucleoli also increased in response to zinc resulting in the synthesis of new protein involved in heavy metal tolerance. This review may help in interdisciplinary studies to assess the ecological significance of metal stress.

Zinc inhibition of cellular energy production: implications for mitochondria and neurodegeneration

Abstract: An increasing body of evidence suggests that high intracellular free zinc promotes neuronal death by inhibiting cellular energy production. A number of targets have been postulated, including complexes of the mitochondrial electron transport chain, components of the tricarboxylic acid cycle, and enzymes of glycolysis. Consequences of cellular zinc overload may include increased cellular reactive oxygen species (ROS) production, loss of mitochondrial membrane potential, and reduced cellular ATP levels. Additionally, zinc toxicity might involve zinc uptake by mitochondria and zinc induction of mitochondrial permeability transition. The present review discusses these processes with special emphasis on their potential involvement in brain injury.

The combined effects of hardness, pH, and dissolved organic carbon on the chronic toxicity of Zn to D. magna: development of a surface response model.

Abstract: The effect of changes in pH, hardness, and dissolved organic carbon (DOC) and the possible interactions among these parameters on the chronic toxicity of zinc to D. magna were investigated. Based on a Central Composite Design, models were developed that can explain the observed variation in EC10 and EC50 as a function of these toxicity modifying factors. All three parameters significantly altered the observed effect concentrations based on net reproductive rate. The largest differences in 21-day EC10s and EC50s caused by these factors were 10.1 and 4.9, respectively. An increase in pH and/or DOC decreased zinc toxicity. The significant interaction between pH and DOC on observed chronic Zn toxicity is in accordance with earlier reported increased sorption efficiency of Zn to humic substances at higher pH levels. Lowest Zn toxicity was observed in tests performed with moderately hard test media (between 200 and 300 mg/L as CaCO3). Lower or higher hardness of the test medium resulted in lower effect concentrations. Based on physico-chemical characteristics of the test media, developed models can be used to explain the variation between reported NOECs for Zn and may improve current environmental risk assessment procedures of metals.

Zinc toxicity on neonatal cortical neurons: involvement of glutathione chelation.

Abstract: Several mechanisms have been implicated in pathological neuronal death including zinc neurotoxicity, calcium excitotoxicity and oxidative injury. Glutathione (GSH) serves to provide reducing equivalents for the maintenance of oxidant homeostasis, and also plays roles in intracellular and intercellular signaling in the brain. We investigated the role of GSH homeostasis in the neurotoxic action of zinc using both mixed cortical cultures containing neurons and glia, and cortical neurons prepared from 1-day-old rats. Zinc caused neuronal cell death in a concentration-dependent manner. In parallel, a high concentration of zinc depleted GSH, in a time-dependent manner, preceding the onset of neuronal damage. Depletion of GSH by diethylmaleate injured neurons and exacerbated zinc-induced death. In contrast, replenishment of GSH attenuated zinc neurotoxicity. The thiol-containing compounds N-acetylcysteine and GSH chemically chelated zinc leading to decreases in the influx of zinc, the fall in GSH level and neuronal death. Interestingly, the glycolytic substrate pyruvate, but not lactate, chelated zinc concentration dependently and prevented its toxicity. On the other hand, pyrrolidine dithiocarbamate, serving as a zinc chaperon, enhanced its entry and toxicity. The results suggest that zinc non-enzymatically depleted GSH, an intrinsic factor for neuron survival, leading to activation of the cellular death signal and eventually neuronal death.

Assessment of the Trace Element Status of Individuals and Populations: The Example of Zinc and Copper

Abstract: This paper describes the proceedings of a workshop that was convened at the 11th International Symposium on Trace Elements in Man and Animals (TEMA-11) symposium to review recent advances concerning the assessment of the trace element status of individuals and populations, using zinc and copper as the primary examples to illustrate basic principles and recent advances in assessment methods. The workshop was initiated with a brief review of the importance of zinc nutriture for human health and a discussion of the likely common occurrence of zinc deficiency worldwide. This overview was followed by presentations on selected issues concerning the assessment of zinc status, with particular attention devoted to dietary assessment techniques, the use of isotopic tracers to assess zinc homeostasis and the relationship of these methods to biochemical indicators of zinc status. Because relatively little information is available on zinc toxicity, the discussion concerning the definition of excess intake of trace elements focused primarily on recent work concerning risk assessment of copper toxicity.

Variability in zinc tolerance, measured as incorporation of radio-labeled carbon dioxide and thymidine, in periphyton communities sampled from 15 European river stretches.

Abstract: Fifteen European rivers and streams belonging to watersheds in Sweden, the Netherlands, and Spain respectively, were sampled by allowing periphyton to colonize submerged glass substrata. Their zinc tolerances were quantified in short-term laboratory tests, where inhibition of photosynthesis in microalgae and thymidine incorporation in bacterial DNA was measured, and expressed as EC50 values. The variability in zinc tolerances was high reaching 1.5–2.5 orders of magnitude, ranging from 25–8145 μM for photosynthesis and 15–467 μM for thymidine assays. Based on the observed variability, uncertainty factors were estimated for the extrapolation of zinc toxicity data from river to river, both regionally and interregionally. Under the assumption to protect 95% of the observed communities the regional uncertainty factors were 1.7–4.3 and the interregional 2.4–8.6. The sampling sites were characterized in terms of biotope physiography, water chemistry, periphyton biomass, trace element content, and species composition. Multivariate analysis of the data using PLS (Projection to Latent Structure), was used to generate hypotheses about the relation between periphyton zinc tolerance and the 123 so-called predictor variables. Zinc contamination, phosphate, nitrogen nutrients, pH, calcium, bicarbonate, dissolved organic carbon, and various diatom species are important predictors for zinc tolerance in the entire data set representing all 15 river stretches. Regional models suggested that very different factors determined the zinc tolerance in the Swedish and Dutch periphyton. The results are interpreted in terms of Pollution-Induced Community Tolerance (PICT) and the bioavailability of zinc.

Zinc‐associated acute pancreatitis in a dog

Abstract: Zinc-induced haemolytic anaemia is a common phenomenon in dogs in the USA following the ingestion of pennies minted after 1982. A case of acute pancreatitis secondary to zinc toxicosis in a dog is described. Acute pancreatitis has been reported in humans, following the ingestion of liquid zinc chloride, but zinc-associated pancreatitis has not been reported previously in the dog. The mechanism of toxicity is unknown, although the pathophysiology may relate to the role of the pancreas in zinc excretion. Acute pancreatitis as a sequela to zinc toxicosis in the dog represents a complication that may prolong hospitalisation and worsen the prognosis.

Involvement of poly ADP ribosyl polymerase-1 in acute but not chronic zinc toxicity.

Abstract: We have previously suggested that zinc-induced neuronal death may be mediated in part by inhibition of the glycolytic enzyme glyceraldehyde-3-phosphate dehydrogenase (GAPDH), secondary to depletion of the essential cosubstrate NAD + . Given convergent evidence implicating the NAD + -catabolizing enzyme, poly ADP ribosyl polymerase (PARP) in mediating ATP depletion and neuronal death after excitotoxic and ischemic insults, we tested the specific hypothesis that the neuronal death induced by exposure to toxic levels of extracellular zinc might be partly mediated by PARR PARP was activated in cultured mouse cortical astrocytes after a toxic acute Zn 2 + exposure (350 μM Zn 2 + for 15 min), but not in cortical neurons or glia after exposure to a toxic chronic Zn 2 + exposure (40 μM Zn 2 + for 1-4 h), an exposure sufficient to deplete NAD + and ATP levels. Furthermore, the neurotoxicity induced by acute, but not chronic, Zn 2 + exposure was reduced in mixed neuronal-glial cultures prepared from mutant mice lacking the PARP gene. These data suggest PARP activation may contribute to more fulminant forms of Zn 2 + -induced neuronal death.

Decreased GSSG reductase activity enhances cellular zinc toxicity in three human lung cell lines.

Abstract: Cellular reduced glutathione (GSH) levels have been identified as an essential determinant in zinc-induced cytotoxicity. However, cytotoxic effects of zinc have also been observed without depletion of GSH stores. In a previous study, the intracellular activity of GSSG reductase (GR) has come into focus (Walther et al. 2000, Biol Trace Elem Res 78:163–177). In the present paper we have tried to address this issue more deeply by inhibiting the activity of cellular GR without any appreciable decreases of cellular glutathione. In three pulmonary cell lines, GR activity was inhibited in a dose-dependent manner by the alkylating agent carmustine (BCNU), a known inhibitor of GR. Cells were pretreated with BCNU for 14 h, followed by exposure to various concentrations of zinc chloride. Then we determined the incorporation of radiolabelled methionine (to assess protein synthesis), and measured the GSH and oxidized glutathione (GSSG) levels. Additionally, GR activity of controls was measured. IC50 values for zinc-induced inhibition of methionine incorporation, as well as GSH contents, was strongly correlated to the decreased GR activity. These results firmly suggest that GR is an important factor in the event chain of zinc cytotoxicity. Together with the results from our previously cited study where impaired regeneration of GSH levels were accompanied by a decrease in total cellular glutathione (GSH + GSSG) we conclude that GSSG itself is an important effector in zinc cytotoxicity.

Neurotoxicity of Dental Amalgam is Mediated by Zinc

Abstract: The use of dental amalgam is controversial largely because it contains mercury. We tested whether amalgam caused toxicity in neuronal cultures and whether that toxicity was caused by mercury. In this study, we used cortical cell cultures to show for the first time that amalgam causes nerve cell toxicity in culture. However, the toxicity was not blocked by the mercury chelator, 2,3-dimercaptopropane-1-sulphonate (DMPS), but was blocked by the metal chelator, calcium disodium ethylenediaminetetraacetate (CaEDTA). DMPS was an effective mercury chelator in this system, since it blocked mercury toxicity. Of the components that comprise amalgam (mercury, zinc, tin, copper, and silver), only zinc neurotoxicity was blocked by CaEDTA. These results indicate that amalgam is toxic to nerve cells in culture by releasing zinc. While zinc is known to be neurotoxic, ingestion of zinc is not a major concern because zinc levels in the body are tightly regulated.

Copper deficiency anemia and nephrosis in zinc-toxicity: a case report.

Abstract: Zinc is a ubiquitous element that is essential for normal enzymatic function in multiple metabolic pathways. Chronic excessive zinc ingestion causes severe reversible anemia in humans. In animals, zinc toxicity leads to anemia as well as physiologic and morphologic damage to the pancreas, kidneys, and often, multisystem failure and death. In this case, a young female ingested approximately 2000 mg of zinc gluconate daily for 12 months. She subsequently developed anemia consistent with zinc-induced copper deficiency and severe nephrosis. After cessation of zinc ingestion, her anemia and nephrosis resolved. This case study underscores the importance of an accurate and thorough investigation of nutritional supplements during the history and physical examination. Given the promulgation of zinc for the treatment of skin disorders and the common cold, along with the commercialization of nutritional supplements, unimpeded by regulatory guidelines, it is imperative that primary care physicians be attuned to the potentially dangerous consequences of excessive zinc ingestion.

Zinc salt compositions for the prevention of mucosal irritation from spermicides and microbicides

Abstract: The addition of low concentrations of combinations of water-soluble organic salts of zinc to gels, creams, lotions or ointments can increase the ability of these products to reduce or prevent exogenous irritants from causing irritation of the underlying substrate. The addition of low concentrations of combinations of water-soluble organic zinc salts to these gels, creams, lotions or ointments also can reduce the irritation of skin or mucous membranes caused by the addition of potentially-irritating substances such as spermicides, microbicides, fungicides or other therapeutic agents to the gel, cream, lotion or ointment. The advantages of this anti-irritant approach over others, which generally employ high concentrations of single zinc salts, are the reduced potential for zinc toxicity, the reduced potential for toxicity related to zinc itself, and the preservation of the desirable biological properties of potentially-irritating therapeutic substances added to the gel, cream, lotion or ointment.

Comparison of Bacterial Bioluminescence with Activated Sludge Oxygen Uptake Rates during Zinc Toxic Shock Loads in a Wastewater Treatment System

Abstract: The use of a bioengineered bioluminescent bacterium (Shk1) for monitoring zinc toxicity was evaluated with samples from a municipal activated sludge wastewater treatment plant and in a bench-scale ...

Effects of cadmium and zinc toxicity on orientation behaviour of Echinoparyphium recurvatum (Digenea: Echinostomatidae) cercariae

Abstract: The effects of cadmium and zinc toxicity on orientation behaviour (photo- and geo-taxis) of Echinoparyphium recurvatum cercariae was investigated at concentrations ranging from 10 to 1000 microg l(-1). Exposure to the toxicants at all metal concentrations caused a change in orientation to negative phototaxis and positive geotaxis during the submaximal dispersal phase (0.5 h cercarial age). Autometallography staining of cercariae exposed to 1000 microg l(-1) cadmium or zinc showed selective binding of heavy metals to tegumental surface sites associated with sensory receptors. The significance to parasite transmission of changes in cercarial orientation behaviour in metal polluted environments is discussed.

Modulation of radish metabolism by zinc phytotoxicity

Abstract: The effect of excess zinc on radish (Raphanus sativus L) cv. Jaunpuri was examined by growing plants in refined sand for 24 days in complete nutrient solution; on 25 t h day zinc as zinc sulphate was added at 0.1 and 0.2 mM (excess) levels. A set of radish plants was also maintained at 0.001 mM Zn and served as control. After 10-12 t h day of metal supply, the visible symptoms as depression in growth and irregular interveinal chlorosis of mature young leaves of zinc toxicity were observed with 0.2 mM Zn. With ageing, growth almost ceased and chlorosis intensified covering entire lamina, later brown necrotic spots appeared on chlorotic areas, enlarged, coalesced and whole leaf turned necrotic and limped down. These effects were more severe at 0.2 than 0.1 mM Zn. After 40 days of treatments, excess zinc reduced the root development, fresh weight, biomass of radish, concentration of total as well as active iron, chlorophylls a and b and activity of catalase, peroxidase, acid phosphatase and starch phosphorylase in leaves. In radish the accumulation of zinc was more in tops than in roots with application of zinc.

The role of oxidative stress on the effect of 1,4,7,10,13,16-hexathiacyclooctadecane on copper and zinc toxicity in HepG2 cells

Abstract: Experiments have shown that 1,4,7,10,13,16-hexathiacyclooctadecane (L3) increased the Cu2+ toxicity on HepG2 cells, whereas the combination Zn(2+)/L3 was less toxic relative to the metal control. In all cases, glutathione (GSH) levels were decreased and vitamins C and E supplementation partially counteracted the increased toxicity in the Cu(2+)/L3-treated cells. The previously observed effects of this hexathiamacrocyclic ligand (L3) on the Cu2+ and Zn2+ toxicity were further investigated by first depleting the intracellular GSH levels by means of L-buthionine S,R-sulphoximine. Combined treatment with Cu(2+)/L3 resulted in complete cell death, whereas for Zn(2+)/L3 no severe effects were observed. Direct measurement of reactive oxygen species (ROS) revealed that Cu2+ induced a high degree of oxidative stress on the cells. This was not the case for Zn2+. The results proved a previously proposed mechanism in which GSH is used to conjugate the metal-ligand complex, but as a result of this, GSH is no longer available for inactivation of ROS. Also, both the intracellular copper and zinc content were determined for each experiment by means of inductively coupled plasma-atomic emission spectroscopy. According to these data, zinc is depleted in Cu(2+)/L3-treated cells, which could have consequences on superoxide dismutase and as a result of this on the amount of oxidative stress.

Effects of zinc toxicity on the structure and function of immune system in ducklings

Abstract: Objective: To investigate the influence and mechanism of zinc toxicity on the stucture and function of immune organs in ducks Methods: By establishing the pathological model of zinc toxicity in ducks, some immunological methods, light and electron microscopes were used to check the changes in the stucture and function of immune system Results: (1) The body weight of ZT group was significantly lower than that of ZC group after 3 weeks (P001) (2) Weights of thymus, the bursa of Fabricius after 2 weeks and that of spleen after 3 weeks were decresed significantly in ZT ducks (3) In 4 weeks, the G 0/G 1 phases of cell cycle of thymus, bursa of Fabricius and spleen were significantly higher and S, G 2+M phases lower in ZT group than those in ZC group (4) In ZT grop, ANAE + positive rates of T lymphocytes in peripheral blood in 2 4 weeks were significantly lower than those of ZC group (P001) (5) Compared with controls, in ZT ducks the counts of lymphocyte reduced significantly and lymphocytes lined loosly in the thymus, bursa of Fabricius and spleen histopatologically The ultrastructural observation showed that the mitochondriae in lymphocytes of the thymus, bursa of Fabricius and spleen were damaged and reticular cells consisted of many primary and secondary lysosomes as well as phagocytes in ZT ducks (6) In comparison with the control, the erythocyte C 3bR rosette rates were significantly lower and the erythrocyte ICR rosette rates were significantly higher in ZT ducks (P001) Conclusion: Zinc toxicity greatly hindered the development of immune organs, caused obvious pathological injury of immune organs, and weakened the funcion of humoral, cellular and erythrocyte immunity

Zinc Toxicity in Companion and Breeding Parrots

Abstract: An ever increasing amount of information has been discovered through research and case studies involving the heavy metal toxicity caused by ingestion of excess environmental zinc. This brief article attempts to review case literature, discuss sources of environmental zinc, toxic levels and strategies to prevent this life threatening illness. Zinc, a trace element essential for life, can be deadly if present in higher levels in many pet and captive breeding birds. Monopoly game pieces, pennies minted after 1982, galvanized wire and hardware (including nuts, bolts, nails, etc.), some ceramic dishes, staples, fertilizers, and some paints and shampoos can contain enough zinc to induce zinc toxicity in captive birds. Parrots by nature are curious and will often chew on objects that can be toxic. Often, xrays fail to provide definitive identification of the object that induced zinc toxicity, especially if no solid zinc object was ingested. Bird-proofing a home is imperative to minimize the probability of your pct contacting and ingesting potentially deadly amounts of heavy metals. Birds suffering from zinc toxicity may exhibit a wide range of clinical signs including, but not limited to, lethargy, weakness, anorexia, weight loss, anemia, feather picking, and neurological disorders including seizures and behavioral changes. Complicating the diagnosis of this disease, many avian diseases cause similar nonspecific clinical signs as zinc toxicity. CBC and blood chemistry panels are often unremarkable or may indicate mild anemia which may be a finding in any chronic disease process. Further complicating the diagnosis, radiographs may not be indicative of toxicity as in many cases no metallic densities are observed in birds with high zinc levels in the blood. Consequently, the doctor may not investigate zinc as a possible causative agent for the observed clinical signs. Chronic ingestion of small amounts of zinc and radiographically visible zinc objects can result in zinc toxicosis. Since radiography, CBC and blood chemistry panels can yield false negatives in patients suffering from zinc toxicosis, many cases go undiagnosed and, therefore, untreated. Another caveat to consider during the diagnosis of this malady is that many birds with high serum levels of zinc do not show clinical signs. Less obvious problems such as decreased fertility may be incorrectly attributed to factors other than environmental zinc toxicosis with potentially disastrous financial consequences for the breeder. Successful chelation therapy for zinc toxicity and removal of continued exposure to zinc sources have demonst~ated increased fertility rates in breeding pairs. Aggression can be caused by high blood zinc levels and may prove to be very problematic for the pet owner. In some cases it may even result in relocation of the affected bird. In some cases, apparently healthy birds have died without ever exhibiting any signs of disease or injury. Some of these cases may have been caused by zinc induced neurologic dysfunction resulting in fatal head trauma fromflying into a cage wall enclosure. It is often difficult to definitively diagnose head trauma as a cause of death post mortem. In a study of a group of 77 Orange-bellied parrots (Neophema chrysogaster) that were found to have died from zinc toxicity over a period of time in a single aviary, the majority had neither prior clinical illness nor exhibited poor body condition. The histologic lesions characteristic of zinc toxicity were absent during necropsy, suggesting an acute toxicity, since research has revealed a one to two week time lapse between zinc ingestion and appearance of characteristic lesions. In this particular case, blood zinc levels were overlooked resulting in the inability to determine the cause of death. Until a few cases with characteristic lesions in the kidneys and other organs were discovered, researchers had not considered zinc as a possible cause for the unexplained deaths. When the cage enclosures were changed from galvanized steel wire to nylon mesh, the incidence of sudden death induced by zinc toxicosis disappeared. Also, the fertility of the birds increased from 54% to 86% in four months. Zinc blood levels are accurately determined with a blood sample and appropriate analysis. Since zinc can leach into a rubber syringe or vial stopper, the sample must be collected in a special vial using a syringe that does not have a rubber stopper. This procedure prevents inaccurately low levels of zinc in the blood analysis. Your avian veterinarian can easily take the sample and refer it to a laboratory that is equipped for testing zinc levels. Typically, levels should be less than 2.0 ppm (200µg/dl), but this can vary from species to species. Ingested zinc is absorbed via the gastrointestinal tract and distributed to tissues and organs including the liver, kidneys, pancreas, reproductive organs, and blood plasma. Since zinc interferes with pancreatic cellular protein synthesis, the pancreas is the most probable target organ and cell necrosis can result. Fortunately, various treatment methodologies for zinc toxicity exist. Chelation therapy using calcium EDTA, d-penicillamine, 2,3 dimercaptosuccinic (DMSA), and dimercaprol (BAL) may be successful in lowering blood zinc to acceptable levels.