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: Two competing mechanisms appear to operate: as the pH rises, dissolved zinc becomes increasingly toxic, but at higher pH levels it is increasingly replaced by zinc precipitate, which is of very low toxicity to fish.
Abstract: The acute lethality of dissolved zinc to rainbow trout (Salmo gairdneri) was significantly increased at higher pH and lower hardness levels. Changes in pH from 5.5 to 7.0 increased zinc toxicity by...
93 citations
TL;DR: Results suggest that the ROS, protein phosphatase and PI-3K may function in the Zn-induced cellular toxicity in rice roots.
Abstract: Cell death in rice roots due to zinc (Zn) toxicity was investigated using inhibitors of signal molecules known to regulate programmed cell death in plants. Zn (5.0– 25.0 mM) induced cell death in a dose- and time-dependent manner. Sodium benzoate, a scavenger of reactive oxygen species (ROS), increased the cell viability under toxic Zn level (25.0 mM), suggesting a role of ROS in Zn-induced cell death. The protective role of rotenone in cell death indicated the involvement of mitochondrial electron transport chain in this Zn-induced ROS generation. Cantharidin and endothall, two serine/threonine phosphatase inhibitors, and sodium orthovanadate (Na3VO4) and phenylarsine oxide (PAO), two protein tyrosine phosphatase inhibitors, blocked Zn-induced root cell death. Conversely, K252-a, a serine/threonine kinase inhibitor, increased Zn-induced cell death. Furthermore, the phosphatidylinositol 3-Kinase (PI-3K) inhibitors, LY 294002 and wortmannin inhibited Zn-induced root cell death. These results suggest that the ROS, protein phosphatase and PI-3K may function in the Zn-induced cellular toxicity in rice roots.
93 citations
TL;DR: In this article, the effect of zinc toxicity on photosystem II (PSII) activities, photosynthetic function, and some mineral concentrations in hydroponically-grown Lolium perenne was studied at four ZnSO4 concentrations (1, 5, 10, and 20 mmol/L) in the nutrient solution.
92 citations
17 Sep 2004
TL;DR: In this paper, the role of ZnT-1 in reducing zinc-dependent cell damage in astrocytes was assessed, and the effect of pre-treatment with sub-lethal concentrations of zinc was demonstrated.
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 ∼200 μM 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
92 citations
91 citations