Showing papers on "Zinc toxicity published in 1997"
TL;DR: The joint toxic effect of copper and zinc for E. crypticus was of similar magnitude as found in studies with aquatic species exposed to metal mixtures, as a result of dissimilarity between total and bioavailable concentrations.
97 citations
TL;DR: The overall effects of zinc intoxication on the various organ systems, possible hematological derangement, and the impairment of copper absorption as well as the outcome with treatment are discussed.
Abstract: This is the first reported case of human fatality associated with zinc intoxication following a massive ingestion of coins. Four hundred and sixty-one coins were removed form the gastrointestinal tract of a schizophrenic patient during the course of hospitalization. Many of the post-1981 pennies, which consist primarily of zinc, showed severe corrosion due to their prolonged contact with acidic gastric juice. The patient presented with clinical manifestations consistent with the local corrosive as well as systemic effects of zinc intoxication and died 40 days after admission with multi-system organ failure. Tissue samples of the kidneys, pancreas, and liver obtained at autopsy revealed acute tubular necrosis, mild fibrosis, and acute massive necrosis, respectively, and contained high levels of zinc. The overall effects of zinc intoxication on the various organ systems, possible hematological derangement, and the impairment of copper absorption as well as the outcome with treatment are discussed.
87 citations
TL;DR: In this paper, the influence of temperature on the ecotoxicity of zinc was evaluated, where the springtail Folsomia candida was exposed to zinc-contaminated soil at different temperatures.
58 citations
TL;DR: Toxicity of sediments from Manitouwadge Lake, Ontario, to Hyalella correlated closely with bioaccumulation of zinc but not copper, suggesting that toxicity is due to zinc itself and not some other chemical that correlates with zinc in sediments.
Abstract: Toxicity of sediments from Manitouwadge Lake, Ontario, to Hyalella correlated closely with bioaccumulation of zinc but not copper. Bioaccumulation in 1-week exposures was sufficient to infer chronic zinc toxicity. Close similarity between toxicity-accumulation relationships from Manitouwadge Lake and those obtained from zinc-spiked Hamilton Harbour sediments indicate that toxicity is due to zinc itself and not some other chemical that correlates with zinc in sediments. Sediment concentrations of zinc, on the other hand, are unreliable indicators of effects; toxicity was not highest in sediments from the most contaminated site. Copper accumulation was insufficient to cause short-term (1-week) toxicity. Chronic copper toxicity cannot be predicted from bioaccumulation, but the absence of a significant growth reduction, which is specific to copper, strongly suggests that the contribution of copper to chronic toxicity was minimal. Body concentrations of zinc and copper in wild animals from contaminated lakes (...
32 citations
TL;DR: The results led to the conclusion that the phloem transport was strongly inhibited above a critical zinc level and that this effect was most likely due to interference withphloem loading or with the mass flow in the sieve tubes and not primarily by affecting phloems unloading or metabolism in the sinks.
30 citations
TL;DR: It is proposed that an interaction with ion channels may play a key mechanism in the processes of apoptosis affecting the vestibular hair cells, and that zinc enhances aminoglycoside ototoxicity.
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.
10 citations