Topic
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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TL;DR: Mortality of newly-hatched fry was seen to be the most sensitive parameter as compared with factors such as number of deposited eggs, hatch-ability, and the mortality of underyearlings, yearlings, and mature minnows.
Abstract: The long-term effects of zinc nitrate on the reproduction and on the mortality during different developmental stages of the minnow,Phoxinus phoxinus L., have been studied in fresh water. Mortality of newly-hatched fry was seen to be the most sensitive parameter as compared with factors such as number of deposited eggs, hatch-ability, and the mortality of underyearlings, yearlings, and mature minnows. The fry showed an increased mortality at a zinc concentration of 0.08 ppm, which is 1/40 of the 96-hr LC50 estimated for the adults.
23 citations
TL;DR: Multi-omics analysis combined with additional experimental evidence suggests Zn intoxication induces ferroptosis, an iron and lipid peroxidation-dependent programmed cell death, demonstrating the utility of multi-omicsAnalysis to identify cellular response to intoxicants.
Abstract: Zinc (Zn) is an essential trace metal required for all forms of life, but is toxic at high concentrations. While the toxic effects of high levels of Zn are well documented, the mechanism of cell death appears to vary based on the study and concentration of Zn. Zn has been proposed as an anti-cancer treatment against non-small cell lung cancer (NSCLC). The goal of this analysis was to determine the effects of Zn on metabolism and cell death in A549 cells. Here, high throughput multi-omics analysis identified the molecular effects of Zn intoxication on the proteome, metabolome, and transcriptome of A549 human NSCLC cells after 5 min to 24 h of Zn exposure. Multi-omics analysis combined with additional experimental evidence suggests Zn intoxication induces ferroptosis, an iron and lipid peroxidation-dependent programmed cell death, demonstrating the utility of multi-omics analysis to identify cellular response to intoxicants.
23 citations
TL;DR: It is concluded that reduction of GSSG is reduced in zinc-exposed cells, and protection of GSH oxidation by various antioxidants as well as enhancement of G SH content are expected to be mechanisms of diminishing toxic cellular effects after exposure to zinc.
Abstract: In a previous work, it was shown that in cells after a decrease of cellular glutathione content, toxic zinc effects, such as protein synthesis inhibition or GSSG (glutathione, oxidized form) increases, were enhanced. In this study, zinc toxicity was determined by detection of methionine incorporation as a parameter of protein synthesis and GSSG increase in various lung cell lines (A549, L2, 11Lu, 16Lu), dependent on enhanced GSSG reductase activities and changed glutathione contents.
23 citations
TL;DR: It is shown here that zinc binds to tPA and inhibits its activity in a dose-dependent fashion, thus terminating its protease-dependent neurotoxic capacity, and physiological levels of tPA confer protection from elevated free zinc.
23 citations
01 Feb 1972
23 citations