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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.


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Journal ArticleDOI
TL;DR: From the perspective of protective substances of zinc-induced neuronal death as a drug of vascular type of dementia based on studies and other numerous studies, carnosine (beta-alanyl histidine) protected against zinc- induced death of cultured neurons.
Abstract: Recent studies have indicated the significance of zinc in neurodegeneration after transient global ischemia. After ischemia, excess glutamate and zinc, which are released in the synaptic clefts, cause the apoptotic death of the target neurons, and finally lead the pathogenesis of vascular type of dementia. Considering the removal of zinc using zinc-sensitive chelators was effective in the prevention of neuronal death after transient global ischemia, it is highly possible that substances which protect against zinc-induced neuronal death will become a candidate for drugs of vascular type of dementia. Based on this 'zinc hypothesis', we have searched for such substances among various agricultural products including fruits, vegetables, and fishes using our developed in vitro screening system. Among tested, we found that carnosine (beta-alanyl histidine) protected against zinc-induced death of cultured neurons, and have applied for the patent as a drug of ischemia-induced neuronal death and the treatment/prevention for vascular type of dementia (application No. 2006-145857) in Japan. Here, we review the perspective of protective substances of zinc-induced neuronal death as a drug of vascular type of dementia based on our studies and other numerous studies.

33 citations

Journal ArticleDOI
TL;DR: Analysis of cases suggests that potentially toxic zinc concentrations in livers of psittacines can be well below the range considered toxic in chickens (>200 ppm), and important differences occur with respect to genera.
Abstract: Determination of zinc concentration in serum/plasma and tissue of caged and aviary birds is commonly requested by practitioners because of an increased awareness of zinc toxicity. However, interpretation of zinc levels is often based on normal zinc concentrations established for poultry. Also, it is likely that intergenus differences exist in normal zinc concentrations of pet birds. In an attempt to determine normal and toxic concentration ranges, zinc concentrations in liver (n = 276) and serum/plasma (n = 260) collected from psittacines between 1990 and 1998 were analyzed. Zinc concentrations were determined by inductively coupled argon plasma emission spectroscopy analysis. The results were categorized by genus and, when available, by history. Birds that were diagnosed with zinc toxicosis (on the basis of history, clinical examination, pathology, and laboratory findings) were exempt and not included in establishing normal ranges. The results indicate that important differences occur with respect to genera. For example, cockatoos and Eclectus parrots have higher normal zinc concentrations in serum or plasma than other psittacines. In addition, analysis of all the submitted cases suggests that potentially toxic zinc concentrations in livers of psittacines can be well below the range considered toxic in chickens (> 200 ppm).

33 citations

Journal ArticleDOI
TL;DR: In vitro, zinc toxicity involved the generation of reactive oxygen species and the activation of the MAP-kinase pathway, and it was concluded that Erk was downregulated, while p38 was stimulated.
Abstract: Zinc is an important component of proteins essential for normal functioning of the brain. However, it has been shown in vitro that this metal, at elevated levels, can be toxic to cells leading to their death. We investigated possible mechanisms of cell death caused by zinc: firstly, generation of reactive oxygen species, and secondly, the activation of the MAP-kinase pathway. Cell viability was assessed by means of the methyl-thiazolyl tetrazolium salt (MTT) assay and confirmed by tetramethylrhodamine methyl ester (TMRM) staining. We measured the phosphorylation status of Erk and p38 as indicators of MAP-kinase activity, using Western Blot techniques. A time curve was established when neuroblastoma (N2α) cells were exposed to 100 μM of zinc for 4, 12, and 24 h. Zinc caused a significant reduction in cell viability as early as 4 h, and indirectly stimulated the accumulation of reactive oxygen species as determined by 2.7 dichlorodihydrofluorescein diacetate (DCDHF) staining and confocal microscopy. Investigation of the MAP-kinase pathway indicated that Erk was downregulated, while p38 was stimulated. Our results therefore led us to conclude that in vitro, zinc toxicity involved the generation of reactive oxygen species and the activation of the MAP-kinase pathway.

33 citations

Journal ArticleDOI
TL;DR: Homeostatic crosstalk between the plasma membrane and intracellular zinc transporters is demonstrated and it is suggested that attenuating zinc influx may enhance β-cell survival.

33 citations

Journal ArticleDOI
TL;DR: In this article, randomized duplicate continuous flow bioassays were made to determine the effect of three dissolved oxygen concentrations on subacute zinc toxicity to bluegills, and the 20-day median tolerance limits (TL m ) at various oxygen concentrations were significantly different at the 95 per cent level of confidence.

33 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
202312
202221
202114
202021
201917
201818