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.

Oxidative stress in newly-hatched Chorthippus brunneus--the effects of zinc treatment during diapause, depending on the female's age and its origins.

Abstract: The responses of glutathione, glutathione S-transferases (GSTs), and catalase (CAT) were determined in 1-day-old larvae of Chorthippus brunneus Thunberg, 1815, a grasshopper exposed to zinc during diapause, from unpolluted (Pilica) or polluted (Olkusz, Szopienice) sites. The aim of the work was to search for differences among populations of the insects as a result of various multistress pressures in their habitats. The question of zinc toxicity in the context of energy allocation was also considered. Zinc caused a decrease in glutathione concentration in the body of zinc-treated larvae. Significant differences between control and zinc-treated groups were confirmed for young females' progeny from Pilica and Olkusz as well as old females' progeny from Olkusz. GSTs activity was generally not influenced by zinc. It is possible that GSTs were not the most important target of zinc action. On the contrary, the influence of zinc on CAT activity was found. The increase in CAT activity after zinc treatment was similar for all studied populations. An increase in CAT activity after zinc exposure seems to be the most universal reaction. CAT activity in zinc-treated grasshoppers may explain the mechanism of zinc toxicity based on reactive oxygen forms generation.

Involvement of raf-1/mek/erk1/2 signaling pathway in zinc-induced injury in rat renal cortical slices

Abstract: Zinc is an essential nutrient that can also be toxic. We have previously reported that zinc-related renal toxicity is due, in part, to free radical generation in the renal epithelial cell line, LLC-PK(1) cells. We have also shown that an MEK1/2 inhibitor, U0126, markedly inhibits zinc-induced renal cell injury. In this study, we investigated the role of an upstream MEK/ERK pathway, Raf-1 kinase pathway, and the transcription factor and ERK substrate Elk-1, in rat renal cortical slices exposed to zinc. Immediately after preparing slices from rat renal cortex, the slices were incubated in medium containing Raf-1 and MEK inhibitors. ERK1/2 and Elk-1 activation were determined by Western blot analysis for phosphorylated ERK (pERK) 1/2 and phosphorylated Elk-1 (pElk-1) in nuclear fractions prepared from slices exposed to zinc. Zinc caused not only increases in 4-hydroxynonenal (4-HNE) modified protein and lipid peroxidation, as an index of oxidant stress, and decreases in PAH accumulation, as that of renal cell injury in the slices. Zinc also induced a rapid increase in ERK/Elk-1 activity accompanied by increased expressions of pERK and pElk-1 in the nuclear fraction. A Raf-1 kinase inhibitor and an MEK1/2 inhibitor U0126 significantly attenuated zinc-induced decreases PAH accumulation in the slices. The Raf-1 kinase inhibitor and U0126 also suppressed ERK1/2 activation in nuclear fractions prepared from slices treated with zinc. The present results suggest that a Raf-1/MEK/ERK1/2 pathway and the ERK substrate Elk-1 are involved in free radical-induced injury in rat renal cortical slices exposed to zinc.

Effect of arbuscular mycorrhizal (G. etunicatum) fungus on antioxidant enzymes activity under zinc toxicity in lettuce plants.

Abstract: Zinc is one of the eight trace elements which are essential for the normal healthy growth and reproduction of crop plants. Plants possess cellular mechanisms that may be involved in the detoxification of heavy metals and thus confer plants a better tolerance against them. Arbuscular mycorrhizal fungi colonization is one of these mechanisms. Here, the effect of mycorrhizal fungus G. etunicatum on Zn toxicity tolerance through enhanced activity of some of antioxidant enzymes has been studied. Treatments were applied in triplicates of two factorial analyses: (a) mycorrhizal and non-mycorrhizal; (b) 5 levels of Zinc (0, 1.5, 3.5, 5.5, 7.5 mM). Zinc was added to modified Hoagland's nutrient solution (with half P concentration). Plants were grown in growth chamber for 10 weeks. Toxicity symptoms such as necrosis and chlorosis appeared on the leaves. Activity of detoxifying enzymes Guaiacol peroxidase (GUPX) and Ascorbate peroxidase (APX) were measured. GPX activity in roots and shoots of mycorrhizal and non-mycorrhizal plants was increased. Also, APX activity increased in roots and shoots ofmycorrhizal and non-mycorrhizal plants. Root length colonization (RLC) was measured by gridline intersect method. Mycorrhizal colonization decreased due to Zinc exposure. The results indicate the probable role of arbuscular mycorrhizal colonization in stress tolerance.

NAP Protects against Tau Hyperphosphorylation Through GSK3

Abstract: Background The most common form of dementia is Alzheimer's disease (AD), which is characterized, in part, by the accumulation of neurofibrillary tangles (NFT), followed by synaptic and neuronal loss. NFTs are mainly composed of aggregated hyperphosphorylated Tau. It has been demonstrated that pathological concentrations of zinc induce 1] activation of a major Tau kinase - the glycogen synthase kinase-3β (GSK-3β), and 2] promote Tau aggregation and toxicity. Activity-dependent neuroprotective protein (ADNP) and its derived peptide NAP exhibit neuroprotective properties against a variety of toxic insults, including toxic zinc concentrations. ADNP deficiency results in increased content of the GSK-3β active form, Tau hyperphosphorylation and NFTlike structure formation, all of which have been prevented by NAP treatment. Our previous experiments showed that NAP enhanced Tau-microtubule association in the face of zinc toxicity. Interestingly, NAP protection against zinc toxicity was rescued by Tau overexpression in NIH-3T3 fibroblast cells, which naturally does not express high amounts of Tau. Objectives and methods Pheochromocytoma cells (PC12), exposed to high concentration of zinc (400µM), were used to determine the protective effect of NAP on Tau phosphorylation and two Tau kinases (Fyn and GSK-3β). Knockdown of Tau expression in PC12 cells by RNA silencing was used to determine Tau's requirement for the NAP protective activity under zinc intoxication. Results NAP treatment attenuated Tau hyperphosphorylation and GSK-3β increased activity caused by zinc intoxication. Furthermore, Tau knockdown completely abolished NAP protective activity. Conclusion These results together with the previous findings strongly corroborated Tau's involvement in NAP/ADNP cellular activity.

Zinc Poisoning - Symptoms, Causes, Treatments.

Abstract: Zinc poisoning has been reported from many parts of the world. It is one of the global health problems that affect many organs, if exposed by inhalation of zinc vapors or by consumption of contaminated food and water. Long term exposure to zinc compounds from different sources such as air, water, soil, and food, lead to toxic effects on body systems, especially digestive, respiratory, and nerve systems, and also causes cancer. Zinc levels can be determined in blood, urine, hair, and nails. Patients with zinc toxicity need chelating agents, other pharmacological treatment, protective lung ventilation, extracorporeal membrane oxygenation (ECMO), and supportive care.