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.

An Autopsy Technique for Zinc-caused Fish Mortality

Abstract: An autopsy method for acute zinc toxicity in fish has been developed. The method is based on the accumulation of zinc in the gills that precedes death due to acute exposure to zinc in the water. Thirty- to 90-day exposures to sublethal concentrations of zinc in water indicated that the opercular bone accumulates zinc at approximately the same rate as the gill tissue (including rakers and arch) but the operculum does not accumulate zinc as the gill does in acutely toxic exposures. By using the ratio of zinc in the gill to zinc in the bone (gill/bone ratio), a reasonably constant value is obtained for nonlethal exposures and for fish collected in the field. This value increases up to a hundredfold in acute exposures. Experimental exposures on five species of fish were made and the fish autopsied. Field samples of more than 1,000 fish of 22 species were analyzed and the data given. There is almost no overlap between the gill/bone ratios of normal fish from the field and experimental fish killed by z...

The effect of zinc-supplemented bread consumption on school children with asymptomatic zinc deficiency.

Abstract: BACKGROUND Zinc deficiency has been seen in developing countries in which grain-based vegetable protein is consumed more often than animal protein. This study was done to emphasize the importance of zinc-fortified foods and to investigate bioavailability of zinc in zinc-fortified bread. METHODS Serum zinc concentrations in healthy 7- to 11-year-old school children were determined. In 24 of 101 children serum zinc concentrations were below 65 micrograms/ul. These 24 children with asymptomatic zinc deficiency were divided into two equal groups. The 12 children with low serum zinc concentrations received the zinc-fortified bread providing 2 mg/kg/day elemental zinc acetate for 90 days (zinc-supplemented group), whereas the other 12 children received the same quality bread with no zinc fortification (control group). RESULTS By the end of the period, the zinc-supplemented group had significantly higher serum and leukocyte zinc concentrations (p < 0.01) and the weight, serum albumin levels, and alkaline phosphatase increased (p < 0.01). Immune functions improved, evidenced by conversion of delayed hypersensitivity skin reactions. Zinc-fortified bread (2 mg/kg/day) caused no side effects or manifestations of zinc toxicity. CONCLUSIONS The results indicate that the bioavailability of zinc in the bread is satisfactory. The use of zinc-fortified bread was found to be an economical and readily accessible method to eliminate zinc deficiency and to prevent further occurrence.

Zinc Toxicity and Iron-Sulfur Cluster Biogenesis in Escherichia coli.

Abstract: While zinc is an essential trace metal in biology, excess zinc is toxic to organisms. Previous studies have shown that zinc toxicity is associated with disruption of the [4Fe-4S] clusters in various dehydratases in Escherichia coli Here, we report that the intracellular zinc overload in E. coli cells inhibits iron-sulfur cluster biogenesis without affecting the preassembled iron-sulfur clusters in proteins. Among the housekeeping iron-sulfur cluster assembly proteins encoded by the gene cluster iscSUA-hscBA-fdx-iscX in E. coli cells, the scaffold IscU, the iron chaperone IscA, and ferredoxin have strong zinc binding activity in cells, suggesting that intracellular zinc overload inhibits iron-sulfur cluster biogenesis by binding to the iron-sulfur cluster assembly proteins. Mutations of the conserved cysteine residues to serine in IscA, IscU, or ferredoxin completely abolish the zinc binding activity of the proteins, indicating that zinc can compete with iron or iron-sulfur cluster binding in IscA, IscU, and ferredoxin and block iron-sulfur cluster biogenesis. Furthermore, intracellular zinc overload appears to emulate the slow-growth phenotype of the E. coli mutant cells with deletion of the iron-sulfur cluster assembly proteins IscU, IscA, and ferredoxin. Our results suggest that intracellular zinc overload inhibits iron-sulfur cluster biogenesis by targeting the iron-sulfur cluster assembly proteins IscU, IscA, and ferredoxin in E. coli cells.IMPORTANCE Zinc toxicity has been implicated in causing various human diseases. High concentrations of zinc can also inhibit bacterial cell growth. However, the underlying mechanism has not been fully understood. Here, we report that zinc overload in Escherichia coli cells inhibits iron-sulfur cluster biogenesis by targeting specific iron-sulfur cluster assembly proteins. Because iron-sulfur proteins are involved in diverse physiological processes, the zinc-mediated inhibition of iron-sulfur cluster biogenesis could be largely responsible for the zinc-mediated cytotoxicity. Our finding provides new insights on how intracellular zinc overload may inhibit cellular functions in bacteria.

Hematology as Index of Sublethal Toxicity of Zinc in a Freshwater Teleost

Abstract: Zinc is one of the common water pollutants and even a very low concentration of 5 mg/l of zinc may be toxic to aquatic life. Zinc in solution has been found to cause gill damage to rainbow trout. Considering the growing importance of hematological parameters in monitoring physiological responses of fish to toxic substances including heavy metals, an attempt is made in this study to investigate blood dyscrasia that may occur in a fresh water teleost, Colisa fasciatus, after acute exposure to sublethal concentration zinc, as zinc sulphate.

Teratogenesis and low copper status resulting from triethylenetetramine in rats.

Abstract: The teratogenicity of triethylenetetramine (TETA) was studied using the Sprague-Dawley rat. TETA was fed during pregnancy at levels of 0 (control), 0.17, 0.83, or 1.66% in a complete purified diet. The frequency of resorptions and the frequency of abnormal fetuses at term increased with increasing levels of the drug. Maternal and fetal tissue copper levels were significantly lower in the TETA groups than in controls, with levels decreasing in a dose-related manner. Maternal kidney and fetal liver zinc levels increased within the TETA groups in a dose-related manner. Maternal liver iron was increased in the high-dose group compared to controls. Fetal iron concentration and maternal and fetal manganese level were not significantly affected by the drug. These results show that TETA can be a teratogenic agent. Furthermore, the results suggest that the teratogenicity of the drug may be due in part to induction of copper deficiency, and perhaps through induction of zinc toxicity.