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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
01 Nov 2004-Glia
TL;DR: Induction of ZnT‐1 may play a protective role when mild episodes of stroke or seizures are followed by a massive brain insult, indicating that preconditioning protects astrocytes from zinc toxicity.
Abstract: Zinc ions are emerging as an important factor in the etiology of neurodegenerative disorders and in brain damage resulting from ischemia or seizure activity. High intracellular levels of zinc are toxic not only to neurons but also to astrocytes, the major population of glial cells in the brain. In the present study, the role of ZnT-1 in reducing zinc-dependent cell damage in astrocytes was assessed. Zinc-dependent cell damage was apparent within 2 h of exposure to zinc, and occurred within a narrow range of approximately 200 microM. Pretreatment with sublethal concentrations of zinc rendered astrocytes less sensitive to toxic zinc levels, indicating that preconditioning protects astrocytes from zinc toxicity. Fluorescence cell imaging revealed a steep reduction in intracellular zinc accumulation for the zinc-pretreated cells mediated by L-type calcium channels. Heterologous expression of ZnT-1 had similar effects; intracellular zinc accumulation was slowed down and the sensitivity of astrocytes to toxic zinc levels was reduced, indicating that this is specifically mediated by ZnT-1 expression. Immunohistochemical analysis demonstrated endogenous ZnT-1 expression in cultured astroglia, microglia, and oligodendrocytes. Pretreatment with zinc induced a 4-fold increase in the expression of the putative zinc transporter ZnT-1 in astroglia as shown by immunoblot analysis. The elevated ZnT-1 expression following zinc priming or after heterologous expression of ZnT-1 may explain the reduced zinc accumulation and the subsequent reduction in sensitivity toward toxic zinc levels. Induction of ZnT-1 may play a protective role when mild episodes of stroke or seizures are followed by a massive brain insult.

100 citations

Journal ArticleDOI
TL;DR: In this paper, the antibacterial responses of zinc oxide (ZnO) structures against Staphylococcus aureus, Pseudomonas aeruginosa, and Streptococcus pyogenes were investigated.

99 citations

Journal ArticleDOI
TL;DR: It is suggested that increased ATP production may provide the energy required for increased glutathione synthesis at the expense of other energy-requiring processes including cell division.
Abstract: The effect of zinc on cell division, photosynthesis, ultrastructure, respiration, ATP levels, mitochondrial electron-transport chain (ETC)-activity, total thiols and glutathione in the marine diatomNitzschia closterium (Ehrenberg) W. Smith was investigated. Although 65µg Zn 1−1 halved the cell division rate, photosynthesis and respiration were unaffected by zinc concentrations up to 500µg Zn 1−1. Most of the zinc associated with the cells was bound at the cell surface, with only 3 to 4% of this extracellular zinc penetrating the cell membrane. Once inside the cell, zinc exerted its toxicity at a number of sites. Increased ATP production and ETC activity were observed in zinc-treated cells. Zinc also enhanced cellular thiols (SH) and total glutathione, and zinc toxicity was reversible by the addition of thiol compounds such as cysteine. Zinc-thiol binding may be a detoxification mechanism for the cell. It is suggested that increased ATP production may provide the energy required for increased glutathione synthesis at the expense of other energy-requiring processes including cell division. The mechanisms of toxicity of ionic zinc and copper toN. closterium were compared.

99 citations

Journal ArticleDOI
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

Journal ArticleDOI
TL;DR: No haematological or biochemical evidence of zinc toxicity was detected during the period of zinc administration, but further studies of the long-term effects of zinc therapy are required.

98 citations


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