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.

Effect of low level zinc pretreatment on zinc-mediated toxicity in different lung cell lines

Abstract: Reduced toxicity of high zinc exposure was observed after pretreatment of various lung cells with nonlethal zinc concentrations. This effect became significant when various parameters of cytotoxicity were assessed (e.g., inhibition of protein synthesis, depletion of reduced glutathione [GSH], increase of oxidized glutathione [GSSG], release of lactate dehydrogenase [LDH]). Similar protective effects by zinc have already been shown by several investigators for a variety of toxicity studies dealing with cadmium, in vitro and in vivo. Zinc-induced toxicity has been linked to glutathione metabolism and cellular GSH contents. Activity of glutathione reductase (GR) and rates of glutathione synthesis were identified as determinants of zinc (cyto)toxicity. However, these variables were virtually unaffected in our adapted cells. Consequently, another variable appears to be crucial for modulating cellular suscepticibility in zinc pretreated cells. Protection in our cells was achieved by pretreatment with 80–120 µmol/L zinc chloride for 24–72 h, roughly 10-fold more zinc in the medium than is normally found in human plasma. Protection was not observed when the cells were concomitantly exposed to cycloheximide, an inhibitor of protein synthesis, or actinomycin D, an inhibitor of RNA synthesis, but it was found in the presence of amanitin, an inhibitor of mRNA synthesis. It is therefore concluded that the altered zinc tolerance of pretreated cells is not attributable to the induction of metallothionein.

Long‐distance mobile mRNA CAX3 modulates iron uptake and zinc compartmentalization

Abstract: Iron deficiency in plants can lead to excessive absorption of zinc; however, important details of this mechanism have yet to be elucidated. Here, we report that MdCAX3 mRNA is transported from the leaf to the root, and that MdCAX3 is then activated by MdCXIP1. Suppression of MdCAX3 expression leads to an increase in the root apoplastic pH, which is associated with the iron deficiency response. Notably, overexpression of MdCAX3 does not affect the apoplastic pH in a MdCXIP1 loss‐of‐function Malus baccata (Mb) mutant that has a deletion in the MdCXIP1 promoter. This deletion in Mb weakens MdCXIP1 expression. Co‐expression of MdCAX3 and MdCXIP1 in Mb causes a decrease in the root apoplastic pH. Furthermore, suppressing MdCAX3 in Malus significantly reduces zinc vacuole compartmentalization. We also show that MdCAX3 activated by MdCXIP1 is not only involved in iron uptake, but also in regulating zinc detoxification by compartmentalizing zinc in vacuoles to avoid iron starvation‐induced zinc toxicity. Thus, mobile MdCAX3 mRNA is involved in the regulation of iron and zinc homeostasis in response to iron starvation.

Effect of zinc on nectar secretion of Hibiscus rosa -sinensis L.

Abstract: Zinc toxicity in secretory cells caused a range of effects, mainly depending on metal concentration. Low concentrations activated nectary function increasing nectar secretion but secretion was greatly inhibited or stopped entirely by ongoing concentration. Water loss rate of zinc treated flower parts was significantly reduced whereas green sepals were dehydrated more rapidly in comparison to colored petals. The content of zinc, calcium, magnesium and manganese increased mainly in sepals under excess of zinc, but in the secreted nectar this metal was not evident. Morphological changes were observed in mucilage cells concerning the mucilage structure and appearance. The parenchymatic, subglandular cells displayed an early vacuolarization and cytoplasm condensation. Secretory hairs appeared to be thinner, the apical cell folded inwards and plasmolytic shrinkage became severe in all cells. The waxy cuticula showed an increased electron density. A plasmalemma detachment from the external cell walls was observed creating a gap between cell wall and plasmalemma. ER cisterns of all treated nectary hairs dominated the cytoplasm and electron dense deposits were seen within its profiles. A great number of other organelles were also present, showing electron dense deposits in their membranes as well. The vacuome was drastically reduced in all cells, except in the subglandular ones and electron dense membrane remnants were observed.

Influence of salinity on physiological development and zinc toxicity in the marine medaka Oryzias melastigma

Abstract: To determine whether the marine medaka Oryzias melastigma is a suitable model organism for evaluating the effects of environmental chemicals on marine teleosts, we examined the effect of salinity on physiological development and zinc toxicity. Growth as measured by total body length was significantly lower in fresh water compared to brackish water. Reproductive success was also significantly reduced in fresh water, although we observed cells in the pituitary producing gonadotropins such as Gpa (common glycoprotein hormone α), Fshb (follicle stimulating hormone β), and Lhb (luteinizing hormone β) at all salinities. These results indicate that O. melastigma is adaptable to various salinities from fresh to seawater, and brackish water is best for physiological processes including growth performance and reproduction. When zinc was dissolved in saltwater, a white precipitate formed immediately, and the dissolved concentration decreased in the supernatant and increased at precipitate. We performed zinc toxicity tests on early life stage and adult stage in fresh water, brackish water, and seawater. Among adults, the lowest observed effect concentration for mortality in freshwater (15.3 mg/L) was lower than in brackish water (>48 mg/L) or seawater (>48 mg/L). Similarly, among embryos and larvae, the lowest observed effect concentration for mortality in freshwater (4.8 mg/L) was lower than in brackish water (48 mg/L) or seawater (48 mg/L). These results highlight the importance of using marine organisms to evaluate the ecological effects of marine pollutants.

Zinc

Abstract: Zinc is ubiquitous, essential for life, and toxic in excess. If sufficient amounts of zinc are available and the supply of other nutrients is proportionate, adequate homeostasis is also maintained. The richest sources of dietary zinc are oysters and similar seafood. The richest common dietary source of bioavailable zinc is red meat. The risk of zinc deficiency is increased by poverty and social disruption. Foods rich in phytate and other zinc-binding ligands, for example, whole grains and legumes, increase the risk of zinc deficiency. A conservative estimate based on UN Food and Agriculture data found a prevalence of zinc deficiency of about 30%. In nature, low concentrations of available zinc in soil that suppresses plant growth are common. Zinc-containing fertilizers correct this problem. In addition, livestock without access to zinc in soil is at risk of deficiency. This is corrected by access to “salt blocks” or supplemented feed. The physiological consequences of zinc deficiency involve all organ systems. The risk of zinc toxicity is increased by excessive consumption of bioavailable zinc or by exposure to zinc-containing chemicals, as in industry. Excessive intakes of zinc for example in over-the-counter supplements impair copper absorption and copper-dependent functions. Other causes of zinc poisoning include zinc-rich dental products, pathological consumption (pica) of metal particles containing zinc such as coins, and consumption of zinc-contaminated food or drink. However, the risk of toxicity is unlikely when Recommended Dietary Guidelines are not exceeded. Zinc toxicity associated with industry includes flu-like metal fume fever from inhalation of zinc oxide fume. Exposure to highly toxic zinc chloride fume can occur in the industry and from the use of smoke bombs for crowd control. To reduce the risks to workers, there are appropriate regulations and precautions.