Showing papers on "Zinc toxicity published in 1996"
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TL;DR: It is suggested that ZnT‐2 protects zinc‐sensitive BHK cells from zinc toxicity by facilitating zinc transport into an endosomal/lysosomal compartment.
Abstract: A cDNA encoding a second zinc transporter (ZnT-2) was isolated from a rat kidney cDNA expression library by complementation of a zinc-sensitive BHK cell line. The protein predicted from the open reading frame of ZnT-2 cDNA has 359 amino acids and initiates with a CTG codon. It resembles ZnT-1 (a plasma membrane protein that stimulates zinc efflux) in overall topology in that it has six membrane-spanning domains, a histidine-rich intracellular loop and a long C-terminal tail; however, the overall amino acid identity is only 26%. Unlike ZnT-1, which is in the plasma membrane and lowers cellular zinc by stimulating zinc efflux, ZnT-2 is localized on vesicles and allows the zinc-sensitive BHK cells to accumulate zinc to levels that are much higher than non-transformed cells can tolerate. Zinc was visualized within these vesicles with zinquin, a zinc-specific fluorescent probe. The intracellular compartment that accumulates zinc is acidic as revealed by staining with acridine orange or LysoTracker. Prolonged exposure of cells expressing ZnT-2 to zinc causes an accretion of intracellular vesicles. We suggest that ZnT-2 protects these cells from zinc toxicity by facilitating zinc transport into an endosomal/lysosomal compartment.
451 citations
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TL;DR: It is suggested that the lack of a hepatic reservoir of zinc jeopardizes the developing kidney in the MT-null mice, which are more sensitive to dietary zinc restriction, and MT I and MT II can protect against both zinc deficiency and zinc toxicity.
Abstract: Metallothionein (MT)-bound zinc accumulates when animals are exposed to excess zinc and is depleted under conditions of zinc deficiency, suggesting that MT serves as a means of sequestering excess zinc as well as a zinc reservoir that can be utilized when zinc is deficient. To examine the importance of MT for these processes, mice with null alleles of both MT I and MT II genes were created and the zinc concentration and histological appearance of multiple organs assessed. At birth, the hepatic zinc concentration of these MT-null mice was lower than that of wild-type controls (0.27 +/- 0.02 vs. 0.65 +/- 0.11 micromol zinc/g tissue, P < 0.05). During the next 3 wk of suckling zinc-replete (95 micrograms zinc/g diet) dams, the hepatic zinc concentration of controls fell to 0.42 +/- 0.04 micromol/g but was unchanged in the MT-null mice (0.28 +/- 0.04 micromol/g). The most prominent histological anomaly observed at 3 wk of age was the presence of swollen Bowman's capsules in the kidneys of MT-null mice. When nursing MT-null dams were fed a severely zinc-deficient (1.5 microg/g) diet, kidney development in the MT-null pups was retarded as indicated by the retention of the nephrogenic zone and incomplete tubule development. We suggest that the lack of a hepatic reservoir of zinc jeopardizes the developing kidney in the MT-null mice. In addition to being more sensitive to dietary zinc restriction, MT-null mice are more sensitive to zinc toxicity. When adult mice were challenged with a ramping dose of zinc up to a total of 3700 micromol zinc/kg body weight, MT-null mice had a greater incidence of pancreatic acinar cell degeneration compared with control mice despite accumulating less zinc (2.72 +/- 0.46 vs. 1.23 +/- 0.52 micromol zinc/g pancreas, control and MT-null, respectively, P < 0.05). The results of these experiments suggest that MT I and MT II can protect against both zinc deficiency and zinc toxicity.
224 citations
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TL;DR: In this paper, long-term growth and metal uptake experiments and short-term uptake kinetic experiments with the coastal diatom Thalassiosira pseudonana revealed antagonistic interactions between toxic metals (Zn and Cd) and the micronutrient manganese.
Abstract: Long-term growth and metal (Mn and Cd) uptake experiments and short-term uptake kinetic experiments with the coastal diatom Thalassiosira pseudonana revealed antagonistic interactions between toxic metals (Zn and Cd) and the micronutrient manganese. Cd and Zn inhibited algal growth rate only at low Mn ion concentrations, an effect that could be totally accounted for by an inhibition of cellular Mn uptake by the toxic metals and the resultant generation of Mn-deficient cells. Mn and Zn inhibited cellular Cd uptake, indicating reciprocal effects among the metals with respect to uptake. Saturation kinetics modeling of the uptake data was consistent with all three metals competing with each other for binding to the Mn uptake system and with both Cd and Mn being transported into the cell by that system (uptake of Zn was not measured). Mathematical modeling of Mn and Cd uptake data revealed evidence for a Cd efflux system that was induced only at high cellular Cd concentrations and prevented cellular Cd from reaching toxic levels.
183 citations
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TL;DR: In contaminated field sites adjacent to primary zinc smelters, zinc is invariably present in soils at concentrations of at least 50 times that of cadmium, so deleterious effects of mixtures of these metals on populations of Collembola in such sites can be attributed to zinc rather than Cadmium.
114 citations
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TL;DR: The objective of this research was to determine the toxic effects and degradation of pentachlorophenol (PCP) in the presence of zinc in anaerobic propionate systems and found that a combined competitive-uncompetitive inhibition model was the best-fit model in the absence of both PCP and zinc for propionates degradation.
Abstract: The objective of this research was to determine the toxic effects and degradation of pentachlorophenol (PCP) in the presence of zinc in anaerobic propionate systems. Anaerobic toxicity assays (ATA), batch kinetic studies, and biodegradation studies were performed using serum bottles. PCP inhibition was modeled using both uncompetitive and noncompetitive inhibition kinetic models with an inhibition coefficient, K{sub I}, of 0.06 mg/L. Zinc toxicity showed that the competitive inhibition model was the best-fit with a K{sub I} of 1.1 mg/L. A combined competitive-uncompetitive inhibition model was the best-fit model in the presence of both PCP and zinc for propionate degradation. In the biodegradation studies, PCP removals were 72, 64, and 54% with spiked PCP concentrations of 2, 3, and 5 mg/L, respectively. In the presence of zinc, the removal of 2 mg/L and 3 mg/L of PCP decreased to 60% and 53%, respectively. The intermediates of PCP degradation were 2,4,6-trichlorophenol, 2,4-dichlorophenol, 4-chlorophenol, 2,3,5-trichlorophenol, 3,5-dichlorophenol, and 3-chlorophenol; lower concentrations of these intermediates were observed in the presence of zinc.
19 citations
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TL;DR: Atomic absorption spectrophotometric analysis of liver samples revealed toxic hepatic zinc levels in the TPN piglets and sources and tissue levels of zinc should be investigated when necrosis, acinar atrophy, and fibrosis of the pancreas are encountered in young pigs.
Abstract: Two Hampshire-Duroc cross piglets maintained on 100% total parenteral nutrition (TPN) for 3 weeks developed pancreatic epithelial cell necrosis, diffuse acinar atrophy, and marked interstitial fibrosis. In addition, the piglets had severe villus atrophy in the small intestine as a result of TPN. Atomic absorption spectrophotometric analysis of liver samples revealed toxic hepatic zinc levels (513.5 and 491.2 ppm) in the TPN piglets (40-90 ppm in control piglets). Administering TPN bypasses homeostatic control mechanisms regulating zinc absorption at the gastrointestinal level and may reduce pancreatic secretion contributing to the accumulation of zinc in tissues. Intestinal villus atrophy, a sequela to TPN, may have also affected zinc excretion by impairing intestinal flux and desquamation. These factors should be considered in formulating TPN solutions and zinc levels administered must be reduced accordingly to avoid toxicity. Furthermore, sources and tissue levels of zinc should be investigated when necrosis, acinar atrophy, and fibrosis of the pancreas are encountered in young pigs.
17 citations
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TL;DR: Results indicated that zinc pyrithione produced the highest inhibition of cell growth when two cell lines were treated in the two doses tested, and triethanolamine and sodium lauryl sulfate produced a similar cytotoxic effect in Fe cells.
13 citations
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TL;DR: As the numerous challenges presented by the study of zinc in human nutrition are met, more appropriate recommendations for dietary and therapeutic zinc intake are being made.
Abstract: Available evidence suggests that trace elements, such as zinc, once thought to have no nutritional relevance, are possibly deficient in large sections of the human population. Conditioned deficiencies have been reported to result from malabsorption syndromes, acrodermatitis enteropathica, alcoholism, gastrointestinal disease, thermal injury, chronic diseases (eg, diabetes, sickle cell anemia), and in total parenteral nutrition therapy. Awareness that patients with these problems are at risk has led health professionals to focus increasingly on the importance of zinc therapy in the prevention and treatment of deficiency. More recently zinc toxicity and its role in human nutrition and well-being have come under investigation. Reports have focused on the role of zinc toxicity in causes of copper deficiency, changes in the immune system and alterations in blood lipids. As the numerous challenges presented by the study of zinc in human nutrition are met, more appropriate recommendations for dietary and therapeutic zinc intake are being made.
9 citations
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TL;DR: The ability of Malin x Polled Dorset crossbred sheep to tolerate the high copper content in PKC at least during the first 16 weeks of the feeding trial may provide more avenue in the utilization of PKC as a major feed ingredient in sheep.
Abstract: Thirty, 4 month-old male Maim x Polled Dorset crossbred sheep were allocated into 6 groups of 5 animals each. Four groups of animals were stall-fed with basal diet of 90% palm kernel cake (PKC) and 10% grass (G) for 16 weeks. One group of the animal was slaughtered at the end of the 16 weeks feeding trial (PKC group), whilst the other three groups were further fed with either the same diet (PKC+PKC group) or fed with a new diet consisting of 30% corn and 10% fish meals (CF) and grass (60%) either with (PKC+CF+Zn group) or without (PKC+CF group) zinc supplementation (500 mg/g Zn as zinc sulfate) for another 16 weeks and were slaughtered at the end of the feeding trial, The other two groups which act as controls were fed with corn (30%) and fish meals (10%) and grass (60%), and were slaughtered at weeks 16 (CF group) and 32 (CF+CF group) of the trial. The blood, right and left liver, renal cortex and medulla, pancreas, bile and urine of all animals were analysed for copper and zinc contents using an atomic absorption spectrophotometer. The liver and kidney were also fixed in 10% buffered formalin for histopathological examination. The study showed that neither clinical signs nor gross lesions of copper or zinc toxicity were observed throughout the trial. However, the copper concentration in both the right and left liver of PKC fed sheep at weeks 16 and 32 rose to about 3 times that of the controls and remained high in both the PKC+CF and PKC+CF+Zn groups. A similar pattern of copper concentration was observed in the blood. The copper and zinc contents in the renal cortex and medulla, pancreas, bile and urine remained low in all groups. The zinc content in the liver of PKC+CF+Zn group was significantly increased. Histologically, moderate hepatic lesions were observed in the PKC fed sheep at week 32. The lesions were milder in the other groups especially in the PKC+CF+Zn group. No significant renal lesions was recorded in all groups. It was concluded that the usage of dietary zinc supplementation (500 mg/g) in the treatment of PKC toxicity in sheep was unsatisfactory. The ability of Malin x Polled Dorset crossbred sheep to tolerate the high copper content in PKC at least during the first 16 weeks of the feeding trial may provide more avenue in the utilization of PKC as a major feed ingredient in sheep.
2 citations
01 Jan 1996
TL;DR: Atomic absorption spectrophotometric analysis of liver samples revealed toxic hepatic zinc levels in the TPN piglets and sources and tissue levels of zinc should be investigated when necrosis, acinar atrophy, and fibrosis of the pancreas are encountered in young pigs.
Abstract: Two Hampshire-Duroc cross piglets maintained on 100% total parenteral nutrition (TPN) for 3 weeks developed pancreatic epithelial cell necrosis, diffuse acinar atrophy, and marked interstitial fibrosis. In addition, the piglets had severe villus atrophy in the small intestine as a result of TPN. Atomic absorption spectrophotometric analysis of liver samples revealed toxic hepatic zinc levels (5 13.5 and 49 1.2 ppm) in the TPN piglets (40-90 ppm in control piglets). Administering TPN bypasses homeostatic control mechanisms regulating zinc absorption at the gastrointestinal level and may reduce pancreatic secretion contributing to the accumulation of zinc in tissues. Intestinal villus atrophy, a sequela to TPN, may have also affected zinc excretion by impairing intestinal flux and desquamation. These factors should be considered in formulating TPN solutions and zinc levels administered must be reduced accordingly to avoid toxicity. Furthermore, sources and tissue levels of zinc should be investigated when necrosis, acinar atrophy, and fibrosis of the pancreas are encountered in young pigs.