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.

The potentiation of zinc toxicity by soil moisture in a boreal forest ecosystem.

Abstract: Northern boreal forests often experience forest dieback as a result of metal ore mining and smelting. The common solution is to lime the soil, which increases pH, reducing metal toxicity and encouraging recovery. In certain situations, however, such as in Flin Flon, Manitoba, Canada, liming has yielded only moderate benefits, with some locations responding well to liming and other locations not at all. In an effort to increase the effectiveness of the ecorestoration strategy, the authors investigated if these differences in liming responsiveness were linked to differences in toxicity. Toxicity of metal-impacted Flin Flon soils on the oribatid mite Oppia nitens and the collembolan Folsomia candida was assessed, with a view toward identifying the metal of concern in the area. The effects of moisture content on metal sorption, uptake, and toxicity to the invertebrates were also investigated. Toxicity tests with the invertebrates were conducted using either Flin Flon soils or artificial soils with moisture content adjusted to 30%, 45%, 60%, or 75% of the maximum water-holding capacity of the soil samples. The Relative to Cd Toxicity Model identified Zn as the metal of concern in the area, and this was confirmed using validation tests with field contaminated soils. Furthermore, increasing the moisture content in soils increased the amount of mobile Zn available for uptake with the ion exchange resin. Survival and reproduction of both invertebrates were reduced under Zn exposure as moisture level increased. Thus, moisture-collecting landforms, which are often also associated with high Zn concentrations at Flin Flon, have, as a result, higher Zn toxicity to the soil ecosystem because of increases in soil moisture. Environ Toxicol Chem 2015;34:600–607. © 2014 SETAC

Toxic effects of cobalt and zinc to Chlorella pyrenoidosa (26) in soft and hard water.

Abstract: Different concentrations (0.83, 3.33, 10 ppm) of cobalt (cobalt sulphate) and zinc (zinc chloride) were added to bristol media prepared using soft water (addition of 20 mg/l calcium carbonate) and hard water (addition of 400 mg/l calcium carbonate). A known amount of Chlorella pyrenoidosa (26) was inoculated into various media, and the number of Chlorella cells was counted every other day for a period of 8 days. Cobalt and zinc were more toxic in media prepared using soft water than hard water as revealed by the growth rate of C. pyrenoidosa. These results agree with studies elsewhere on other aquatic organisms.

Toxicological characterization of the new water cleaning product and its waste by-product.

Abstract: Water extracts genotoxicity of the coagulant produced from industrial waste (red mud and waste base) and its waste mud remained after waste water treatment by the coagulation/flocculation process were studied. Tests were conducted in order to confirm nontoxicity of this new product prior to commercial production and usage and also to recommend a safe way for a handling and disposal of the remaining waste material. The toxicity investigation included (i) determining frequency of the cell survival, (ii) the Ames assays, (iii) micronucleus assay, and (iv) cell proliferation kinetics (expressed as mitotic index). These techniques were also employed in toxicity testing of the different concentrations of metal salts, zinc chloride, and lead nitrate in this case since these two elements were present in high concentrations in the waste water intended for the purification with the new coagulant. Mixture of metal salts in the concentrations that represent maximum allowed values for water extracts of technological waste was also tested. Two strains of Salmonella typhimurium, TA98, and TA100 were used for determining cytotoxicity and for the Ames test, while the cytogenetic investigations were performed on human peripheral blood lymphocytes. Water extracts of the coagulant and its waste mud did not induce a significant increase of the micronuclei in human peripheral blood lymphocytes. They also did not disturb lymphocyte proliferation kinetics in vitro. As regards lead nitrate it proved not to be cytotoxic on bacterial strains in the tested concentration range (1-100 mg/L), whereas zinc chloride showed cytotoxic effect for the concentrations above 25 mg/L. The Ames test results for the noncytotoxic concentrations of these metals were negative. Comparing to the negative control a significantly higher number of the micronuclei was determined after the treatment of the whole blood with 100 mg/L of zinc chloride, as well as with 10 and 100 mg/L of lead nitrate. A linear, dose dependent increase was obtained for both salts. Similar results were obtained on the basis of the mitotic index.

Cell death caused by the acute effects of aminoglycoside and zinc in the ampullary cristae of guinea pigs

Abstract: We reported that apoptosis occurred in the guinea pig vestibular hair cells after chronic aminoglycoside treatments. In the present study, we used in situ nick-end labeling to determine whether apoptosis was also induced by the acute effects of aminoglycosides in guinea pig ampullar cristae. In addition, we evaluated the effect of zinc supplements upon these ototoxic treatments. After a local application of streptomycin directly to the round window, we found labeled bodies in the vestibular hair cells. The zinc supplement increased the number of labeled bodies resulting in severe hair cell loss. These findings indicate that the acute effects of aminoglycosides also induce apoptosis of the vestibular hair cells, and that zinc enhances aminoglycoside ototoxicity. Consequently, we propose that an interaction with ion channels may play a key mechanism in the processes of apoptosis affecting the vestibular hair cells.