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: The data indicated that higher pH and higher concentrations of Ca and DOC were generally associated with lower toxicity (higher ECx values), which lends further support to the use of the chronic Zn BLM to account for bioavailability of zinc in aquatic risk assessment and the derivation of environmental quality standards.
30 citations
TL;DR: Zinc toxicity analyses in various culture medium conditions demonstrated that the toxicity-reducing effect of serum was due largely and perhaps entirely, to serum albumin, which is apparently due to zinc-albumin binding.
30 citations
TL;DR: In this paper, Holcus lanatus L. ecotypes differing in tolerance to zinc toxicity were grown in Zn-deficient Laffer soil which was amended with Zn to create a range of conditions from Zn deficiency to Zn toxicity.
29 citations
TL;DR: It is reported that under conditions mimicking ischemia in hippocampal neurons – normal calcium plus elevated (> 100 μM) exogenous zinc – mitochondrial dysfunction evoked by glutamate, kainate or direct depolarization is, despite significant zinc uptake, primarily governed by calcium.
Abstract: Zinc has been implicated in neurodegeneration following ischemia. In analogy with calcium, zinc has been proposed to induce toxicity via mitochondrial dysfunction, but the relative role of each cation in mitochondrial damage remains unclear. Here, we report that under conditions mimicking ischemia in hippocampal neurons - normal (2 mM) calcium plus elevated (> 100 μM) exogenous zinc - mitochondrial dysfunction evoked by glutamate, kainate or direct depolarization is, despite significant zinc uptake, primarily governed by calcium. Thus, robust mitochondrial ion accumulation, swelling, depolarization, and reactive oxygen species generation were only observed after toxic stimulation in calcium-containing media. This contrasts with the lack of any mitochondrial response in zinc-containing but calcium-free medium, even though zinc uptake and toxicity were strong under these conditions. Indeed, abnormally high, ionophore-induced zinc uptake was necessary to elicit any mitochondrial depolarization. In calcium- and zinc-containing media, depolarization-induced zinc uptake facilitated cell death and enhanced accumulation of mitochondrial calcium, which localized to characteristic matrix precipitates. Some of these contained detectable amounts of zinc. Together these data indicate that zinc uptake is generally insufficient to trigger mitochondrial dysfunction, so that mechanism(s) of zinc toxicity must be different from that of calcium.
29 citations
01 Jan 2013
TL;DR: Tomato (cultivar PKM -1) plants were raised in pots containing the soil amended with various levels of zinc (control, 50, 100, 150, 200 and 250 mg kg soil) and replicates were maintained for each level.
Abstract: Tomato (cultivar PKM -1) plants were raised in pots containing the soil amended with various levels of zinc (control, 50, 100, 150, 200 and 250 mg kg soil). Five replicates were maintained for each level. 1
29 citations