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 interaction between 65Zn, mercury and selenium in rats (retention, metallothionein, endogenous copper).

Abstract: Interaction of zinc with mercuric chloride and sodium selenite was studied in the rat at the organ and subcellular levels (liver and kidneys) Zinc chloride was administered subcutaneously at dose of 5 mg Zn/kg, mercury chloride into the tail vein at a dose of 05 mg Hg/kg (both metals every other day during 2 weeks) and sodium selenite intragastrically, at doses of 01 mg Se/kg, every day Zinc retention in the rat did not exceed 20% and was unchanged in the presence of mercury An interaction effect was reflected by an increased whole-body retention of zinc by selenium, mercury, and selenium In the presence of selenium no peak of metallothionein-like proteins stimulated by zinc or mercury was found in the soluble fraction of the kidneys The metallothionein level did not differ from that typical for control group animals, too A significant increase in the level of endogenous copper was found only in the kidneys of rats exposed to zinc in the presence of mercury and selenium

Chapter 61 – Zinc

Abstract: Zinc (Zn) is ubiquitous, essential for life, and toxic in excess. When diets provide adequate amounts of bioavailable Zn and intakes of other nutrients are also adequate homeostasis is maintained. When the consumption of bioavailable Zn is insufficient, the risk of deficiency increases. The worldwide prevalence of this phenomenon is at least 20%. Excessive consumption of bioavailable Zn and of exposure to Zn-containing chemicals increase the risk of toxicity. The prevalence of the former is unknown. The latter typically occurs in association with industry; the likelihood is decreased by the use of appropriate precautions. Low available Zn in soil is common and if unmitigated decreases agricultural production. Populations at risk of Zn deficiency are also at risk of other deficiencies. Diets based on cereal and legume products are rich in phytate and other indigestible zinc-binding ligands, and diets based on plant products that are low in Zn, such as roots, tubers, and highly milled rice, are the major causes of human Zn deficiency. Although Zn in animal flesh is highly bioavailable, indigestible Zn-binding ligands in diets suppress its availability. The physiological consequences of Zn deficiency involve all systems. Zinc toxicity is most common after habitual excessive consumption of Zn-containing dietary supplements. Bioavailability of dietary copper (Cu) is suppressed, resulting in deficiency. Inadvertent consumption of Zn-rich dental products over time, and the chronic pica of articles composed of Zn also cause Cu deficiency. Acute gastrointestinal illness can occur after consumption of Zn-contaminated food or drink. Zinc toxicity associated with industry includes flu-like metal fume fever from inhalation of Zn oxide fume. Exposure to highly toxic Zn chloride fume can occur in industry, and from the use of smoke bombs for crowd control.

Toxicokinetics and toxicity of zinc under time-varying exposure in the guppy (Poecilia reticulata)

Abstract: Levels of toxic substances released into the environment are often highly variable and fluctuate over time. The present study deals with a simple type of time-variable exposure, diluted pulse. We determined toxicokinetic parameters of zinc in guppy fish (Poecilia reticulata) and evaluated the applicability of a toxicokinetics-based survival model developed earlier. In the toxicokinetics experiment, zinc was rapidly taken up and released again; the half-life in fish was only 1.5 d. In the toxicity experiments with diluted-pulse exposure, survival leveled off to a baseline level, which in accordance with the model is explained by the dilution of zinc. The model fitted reasonably well for the lower initial concentrations but tended to overestimate survival rates at the higher concentrations. Toxicokinetic parameters estimated from changes in survival were close to values estimated from measured zinc concentrations in water. Elimination rates during pulse exposure varied from 0.434 to 0.488 d(-1) and corresponded very well to the elimination rate during constant exposure (0.463 d(-1)). Ultimate LC50 values were estimated as 6.40 and 9.10 mg/L. These results suggest that toxicity experiments with a simple, time-varying exposure can be used as an alternative to conventional, constant-exposure experiments. Toxicokinetic parameters and toxicological endpoints can still be estimated in static bioassays with decreasing exposure if the concentration in the medium is measured. At the same time, diluted-pulse experiments may simulate exposure from discharges in the field better than constant-exposure experiments.