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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: The current concepts concerning zinc biology, its metabolism and transport into cells, its homeostasis, and its role in the functioning of the human immune and endocrine systems, as well as the biophysical mechanisms of action of zinc ions at elevated concentrations on human blood cells are reviewed and analyzed.
Abstract: In this review the current conceptions concerning zinc biology, its metabolism and transport into the cells, its homeostasis, a role in the functioning of the human immune and endocrine systems, participation in cell signaling and its cytotoxicity, as well as the biophysical mechanisms of action of zinc ions action at the elevated concentrations on human blood cells were analyzed.

20 citations

Journal ArticleDOI
TL;DR: Increased S100A6 levels correlate with both Aβ disaggregation and decrease of Aβ plaque-associated zinc contents in brain sections with AD-like pathology, and may protect from Aβ deposition through zinc sequestration.
Abstract: Evidence has been accumulating that zinc ions can trigger β-amyloid (Aβ) deposition and senile plaque formation in the brain, a pathological hallmark of Alzheimer's disease (AD). Chelating zinc inhibits Aβ aggregation and may hold promise as a therapeutic strategy for AD. S100A6 is an acidic Ca2+/Zn2+-binding protein found only in a small number of astrocytes in the normal brain. However, in the AD brain, S100A6 is highly expressed in astrocytes around Aβ plaques. The role of the astrocytic S100A6 upregulation in AD is unknown. In the present study, we examined the effects of S100A6 on Aβ plaques and intracellular zinc levels in a mouse model of AD. Chronic exposure to zinc increased Aβ deposition and S100A6 expression, both reversible by the zinc chelator clioquinol, in the brains of amyloid precursor protein/presenilin 1 (APP/PS1) transgenic mice. To examine whether exogenous S100A6 could induce Aβ plaque disaggregation through competition for zinc in vitro, we incubated APP/PS1 mouse brain sections with recombinant human S100A6 protein or co-incubated them with human S100A6-expressing cells. Both treatments efficiently reduced the Aβ plaque burden in situ. In addition, treatment with exogenous S100A6 protected cultured COS-7 cells against zinc toxicity. Our results show for the first time that increased S100A6 levels correlate with both Aβ disaggregation and decrease of Aβ plaque-associated zinc contents in brain sections with AD-like pathology. Astrocytic S100A6 in AD may protect from Aβ deposition through zinc sequestration.

20 citations

Journal ArticleDOI
TL;DR: The utility of polydentate chelators in the remediation of metal-contaminated systems is demonstrated and it is demonstrated that although the application of a chelator to metal contaminants may be effective, binding alone cannot be used to predict the level of remediation.

20 citations

Journal Article
TL;DR: Liver, kidney and bone lead concentrations and kidney cadmium concentrations were good "post-mortem" indicators of exposure and blood zinc concentrations and zinc concentrations were not significantly increased.
Abstract: Dairy cattle on a farm located in the vicinity of a lead and zinc-ore processing factory were studied over 21 mo and compared with cattle on a control farm. Mean daily intakes of lead from the diet were 4.3 mg/kg body weight, with great variations; mean daily zinc intakes were 5.6 mg/kg body weight; and mean daily cadmium intakes were 0.064 mg/kg body weight. The 3 major indicators of contamination were blood lead concentrations, with mean values of 50 micrograms/100 ml of blood, zinc protoporphyrin with mean values of 165 micrograms/100 ml blood, and lead concentrations in hair which averaged 10 micrograms/g. Blood zinc concentrations and zinc concentrations were not significantly increased. One cow developed fatal post-partum paralysis. Liver, kidney and bone lead concentrations and kidney cadmium concentrations were good "post-mortem" indicators of exposure.

20 citations


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