Showing papers on "Zinc toxicity published in 1989"
TL;DR: It was possible to suppress the cytotoxicity of zinc by increasing the concentration of either Fe2+ or Ca2+ but not Mg2+, which suggests that a prerequisite for the toxic action of zinc is entry into cells using channels that are shared with iron or calcium.
97 citations
TL;DR: Rainbow trout body mucus dialysed with acidified distilled water at pH 7,5 and 3 experienced ion depletion which was greatest at pH 3 and minimal between pH 7 and 5.
Abstract: Rainbow trout body mucus dialysed with acidified distilled water at pH 7,5 and 3 experienced ion depletion which was greatest at pH 3 and minimal between pH 7 and 5. Mucus Na+ loss is exacerbated in the presence of 1 mg I−1 aluminium as A12(SO4), at pH 5 and 7. Al2(SO4), causes greater depletion of Na+ from mucus than A1C13. A lethal level of zinc (2 mg 1−1) does not deplete mucus Na− or K+, unlike a lethal level of aluminium (1 mg 1−1) at pH 7. The results are discussed in terms of the ionoregulatory role of mucus in heavy metal and acid toxicity.
83 citations
TL;DR: To overcome the problems of metal complexation by chelators such as silicate, iron and EDTA in the assay medium, unsupplemented seawater and buffered synthetic softwater, enriched only with nitrate and phosphate are used for the study of metal toxicities to marine and freshwater algae.
76 citations
TL;DR: Zinc toxicity was positively correlated with decreasing acidity over the pH range 5–7, the metal being most toxic at pH 8–9 where metal complexes predominate, and below pH 5 metal toxicity also increased, irrespective of hardness.
Abstract: Exposure of brown trout, Salmo trutta, to zinc under continuous flow conditions over 96 h showed that both water hardness and pH exert major influences on the toxicity of the metal. 96-h LC50 values for total zinc ranged from <0.14mg 1−1 in alkaline soft water (pH 8; lOmg 1−1 as CaCO3) to 3.20 mg 1−1 in acidic hard water (pH 5; 204 mg 1−1 as CaCO3). A variable reduction in zinc toxicity in hard water compared with soft water over the pH range 4–9 was attributed to high external calcium. Zinc toxicity was positively correlated with decreasing acidity over the pH range 5–7, the metal being most toxic at pH 8–9 where metal complexes predominate. Below pH 5 metal toxicity also increased, irrespective of hardness. Water hardness and pH interacted with zinc toxicity in a complex manner, apparently dependent on physical and chemical transformations of the metal, and as changes in uptake. detoxification and excretion by the fish.
50 citations
TL;DR: In this article, the susceptibility of the parthenogenetic eggs of Daphnia magna to cadmium, zinc, copper, and lead was investigated and the early life stages of D. magna proved to be highly tolerant to heavy metal toxicity in comparison with later stages.
40 citations
TL;DR: Zinc is an indispensable trace element and is a constituent of more than 200 enzymes, which can assure the stability of biological molecules such as DNA, or biological structures such as membranes or ribosomes, which makes it a much more frequent risk than toxicity.
Abstract: Zinc is an indispensable trace element and is a constituent of more than 200 enzymes. It can assure the stability of biological molecules such as DNA, or biological structures such as membranes or ribosomes. It is not surprising, therefore, that, compared with zinc toxicity, zinc deficiency is a much more frequent risk. Few acute toxic effects have been ascribed to zinc and no long-term effects were found after single or prolonged exposure at doses below 1 g/kg of food. Zinc is neither mutagenic nor carcinogenic, although its levels may influence tumor growth. Zinc appears not to be teratogenic but, on the contrary, deleterious action on zinc deficiency on the developing organisms is well documented.
23 citations
TL;DR: The genotoxicity of zinc was examined in 4 short-term mutagenicity assays and the effect of ligand binding of zinc in the in vitro test systems is discussed.
Abstract: The genotoxicity of zinc was examined in 4 short-term mutagenicity assays. Zinc acetate produced dose-related positive responses in the L5178Y mouse lymphoma assay and an in vitro cytogenetic assay with Chinese hamster ovary cells, but was negative in the Salmonella mutation assay and did not induce unscheduled DNA synthesis in primary cultures of rat hepatocytes. Zinc-2,4-pentanedione produced frameshift mutations in Salmonella tester strains TA1538 and TA98, but did not induce unscheduled DNA synthesis in primary cultures of rat hepatocytes. The effect of ligand binding of zinc in the in vitro test systems is discussed.
19 citations
Journal Article•
6 citations
TL;DR: Because of the pilot nature of the study and the possible toxic effects and complications of oral zinc administration, widespread use of zinc in macular degeneration is not now warranted, the authors say.
Abstract: To the Editor. —We read the article by Dr Newsome and colleagues 1 with great interest. It was very exciting to learn that in such a well-designed, well-executed, and well-analyzed controlled study, zinc therapy had such a marked effect on reducing the progression of such an important and debilitating disease as macular degeneration. However, we were dismayed by the authors' emphasis on possible zinc toxicity. In their own terms, their abstract closes with, "Because of the pilot nature of the study and the possible toxic effects and complications of oral zinc administration, widespread use of zinc in macular degeneration is not now warranted." Elsewhere in the report the authors expresspecific concerns about anemia and worsening of cardiovascular disease. Our dismay arises from our team having spent the last 20 years administering zinc in relatively high doses to various types of patients and having a very difficult time identifying toxic effects.
4 citations
TL;DR: Triethylenetetramine is a copper chelator used in the treatment of Wilson’s disease and the teratogenicity of TETA may be due at least partly through induction of zinc toxicity.
Abstract: Triethylenetetramine (TETA) is a copper chelator used in the treatment of Wilson’s disease. It is applied primarily to patients with adverse reactions to D-penicillamine (DPA) (Walshe 1973). DPA influences the metabolism of the essential trace element zinc (Klingberg et al 1976). Several adverse effects including teratogenicity may be caused by the zinc depletion. It was also suggested that the teratogenicity of TETA may be due at least partly through induction of zinc toxicity (Keen et al 1983). However, the affinity of TETA for zinc in vivo was not systematicaly investigated.
1 citations