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.

Comparative toxicity of cadmium, zinc, and mixtures of cadmium and zinc to daphnids

Abstract: Investigations were conducted to determine acute (48-h) effects of cadmium and zinc presented individually and in combination on Ceriodaphnia dubia, Daphnia magna, Daphnia ambigua, and Daphnia pulex. Toxicity tests were conducted with single metals to determine lethal effects concentrations (lethal concentrations predicted for a given percent [x] of a population, LCx value). These were used to derive metal combinations that spanned a range of effects and included mixtures of LC15, LC50, and LC85 values calculated for each metal and species. In single-metal tests, 48-h LC50 values ranged from 0.09 to 0.9 micromol/L and 4 to 12.54 micromol/L for cadmium and zinc, respectively. For each metal, D. magna was most tolerant and showed a different pattern of response from all others as determined by slope of concentration-response curves. In the combined metal treatments, all daphnids showed a similar pattern of response when LC15 concentrations were combined. This trend continued with few exceptions when LC15 concentrations of cadmium were combined with LC50 or LC85 values for zinc. However, when this treatment was reversed (LC15, zinc + LC50 or LC85, cadmium), responses of all species except D. magna indicated less-than-additive effects. For C. dubia, a near complete reduction in toxicity was observed when the LC15 for zinc was combined with LC85 for cadmium. Multimetal tests with D. magna did not differ from additive. Collectively, these studies suggest that D. magna may not be representative of other cladocerans.

Comparison of the toxicity and distribution of cadmium and lead in plant cells.

Abstract: The toxicity of heavy metals (Cd, Zn, and Pb) was assessed by in vivo observations of their effect on cytoplasmic streaming in Allium cepa L. bulb scale epidermal cells. On the basis of our results, the order of toxicity of the studied cations is Zn < Pb ≪ Cd. The difference in toxicity between cadmium and lead was found to be very large. When cytoplasmic streaming was assessed, this difference was threefold. When the total content of cadmium and lead (determined by inductively coupled plasma mass spectrometry) was the criterion, the difference in toxicity was 15-fold. Fractionation of the tissue and enzymatic digestion of the cells revealed that the largest proportion of cadmium was located in the cell walls (56%), whereas almost all of the lead (97.6%) was accumulated in an insoluble form. The speciation of water-soluble Pb and Cd fractions is discussed on the basis of analysis by capillary zone electrophoresis interfaced with inductively coupled plasma mass spectrometry of water extracts from epidermal cells. Lead and cadmium appeared to be bound mainly to salts, which explains their toxicity. Cadmium was complexed (detoxified) by organic acids, while thiols were the metal-complexing species for lead. Histidine formed complexes with both cadmium and lead. Ultrastructural analyses showed that lead was encapsulated in small vesicles in the cytoplasm. Fluorescence studies of the endoplasmic reticulum (ER) revealed that it underwent extensive fragmentation under the influence of lead, with numerous ER vesicles appearing in the cells. In other words, the lead deposits in the cytoplasm were contained in vesicles arising from fragmentation of the ER. These observations indicate that epidermal cells have a rapid and effective mechanism for detoxifying lead involving the ER, and this may be one of the mechanisms accounting for the lower toxicity of lead in comparison with cadmium. The suitability of Allium cepa bulb scale epidermal cells for use in ecotoxicological studies is also discussed. Step-by-step directions for this test are given.

Zinc Toxicity in the Mallard Duck

Abstract: Levels of zinc from 3,000 to 12,000 ppm were fed to domestic mallard ducks (Anas platyrhynchos) in their diet. Food intake and body weight both showed closely parallel decreases as the level of zinc in the diet increased. In ducks fed zinc, the pancreas and gonads underwent reductions in relation to body weight, whereas ratios of adrenals and kidneys to body weights increased significantly. No significant change occurred in liver:body weight ratios in ducks fed zinc-supplemented diets. The gonads were so reduced in size that the reproductive function was probably lost. In birds fed zinc-supplemented diets, partial paralysis of the legs, diarrhea, and weight loss were noted within 1!0 days. Severe paralysis, with some ducks unable to waLk, was noted after 20 days. Only slight anemia was present in some ducks after 30 days, but by day 45, extreme anemia (5-13 grams Hb per 100 cc of blood) was evident in most ducks. Normal hemoglobin concentrations averaged 18.6 grams per 100 cc of blood. Significant increases in concerltrations of zinc were found in the liver, kidneys, pancreas, gonads, and breast muscle. High mortality was observed in all groups treated with zinc-supplemented diets; all but 2 of 24 ducks died within 60 days. Paralysis of the legs, high concentrations of zinc in the pancreas and kidneys, and yellowish-red kidneys may be used for diagnosing zinc toxicosis in mallards. Heavy metals such as lead, mercury, copper, and zinc have long been known for their toxicity to animals. Copper and zinc are required as trace elements in the diets of animals, but when they occur in relatively high levels, they become toxic. In this particular set of experiments, toxicity of zinc was studied in domestic mallard ducks to determine the hazard of zinc as an environmental pollutant to waterfowl. This study stems from 70 years of observations, summarized by Chupp and Dalke (1964), of dead and dying ducks, geese, and swans in the Coeur d'Alene Lake area in northern Idaho where zinc is found in high concentrations. The Coeur d'Alene area has been actively mined for at least 70 years and effluents from mines and smelters have been poured into the river systems of the area. These wastes then flow downstream, settling in 1 This investigation was supported by the Society of the Sigma Xi and the senior author's National Defense Education Act Fellowship. 2 Present address: Institute of Arctic Biology, Fairbanks, Alaska. the rivers and lakes, where the aeeumulation of metals beeomes high. Lewis and Deneeke (1923) found 2.86 pereent lead in a sediment sample eolleeted in the Coeur d'Alene valley. Ellis (1940) found a range of 5 to 12 pereent zine in soil enerustations. Chupp and Dalke ( 1964 ) analyzed 12 soil samples (type not stated) and obtained from 150 to 9,600 ppm lead, 240 to 7,700 ppm zine, and 31 to 320 ppm eopper. Three samples of emergent aquatie plants (species not stated) mrere analyzed from which an average of 2,530 ppm lead, 1,930 ppm zine, and 115 ppm eopper were found. As a result, waterfowl that feed in these areas eonsume larger amounts of heavy Inetals than waterfowl feeding in areas of naturally low ( normal ) eoncentrations. Die-offs of dueks, geese, and whistling swans (Olor colaznbianus) have been noted in this area sinee the early 1900's (Chupp and Dalke 1964); however, these die-offs have been variable, oeeurring only in some years. Chupp and Dalke indicated that their tissue analyses for heavy netals and the early studies by the Bureau

Silicon-mediated amelioration of zinc toxicity in rice (Oryza sativa L.) seedlings

Abstract: Background and aims Silicon (Si) was suggested to enhance plant resistance to toxic elements, and its beneficial role was mainly based on external and internal plant mechanisms. This work aimed at investigating the internal effect of Si on zinc (Zn) detoxification to rice (Oryza sativa L., cv. Tian You 116) seedlings. Methods In a hydroponic experiment, we examined the uptake, xylem loading and localization of Zn in rice seedlings under the condition of 200 μ MZ n contamination with the additional silicate supply at three levels ( 0, 0.5 and 1.8 mM). Results The silicate addition significantly increased the seedling biomass, and decreased Zn concentration in both root and shoot of seedlings and in xylem sap flow. Zinpyr-1 fluorescence test and Energy-dispersive X-ray spectroscopy analysis showed the concentration of biologically active Zn 2+ decreased, and Zn and Si co-localized in the cell wall of metabolically less active tissues, especially in sclerenchyma of root. The fractionation analysis further supported silicate supply increased about 10% the cell wall bound fraction of Zn. Conclusions This study suggests the Si-assisted Zn tolerance of rice is mainly due to the reduction of uptake and translocation of excess Zn, and a stronger binding of Zn in the cell wall of less bioactive tissues might also contribute to some degree.

Zinc Transport in the Brain: Routes of Zinc Influx and Efflux in Neurons

Abstract: Studies of the routes of entry and exit for zinc in different tissues and cell types have shown that zinc can use several pathways of exit or entry. In neurons, known pathways include (1) presynaptic release along with glutamate when synaptic vesicles empty their contents into the synaptic cleft, (2) voltage-gated L-type Ca(2+) channels and glutamate-gated channels that provide an entry route when cells are depolarized and that mediate extracellular zinc toxicity and (3) a plasma membrane transporter potentially present in all neurons important for cellular zinc homeostasis. The least understood of these pathways, in terms of mechanism, is the transporter pathway. The kinetics of zinc uptake in cultured neurons under resting conditions are consistent with and suggest the existence of a saturable transporter in the plasma membrane. The proteins responsible for plasma membrane zinc transport have not yet been definitely identified. Likely candidates include two proteins identified by molecular cloning termed zinc transporter 1 and divalent cation transporter DCT1. Both proteins have been shown to be expressed in the brain, but only DCT1 is clearly demonstrated to be a transport protein, whereas zinc transporter 1 may only modulate zinc transport in association with as-yet-unidentified proteins. Understanding the mechanism and neuromodulation of plasma membrane zinc transport will be an important first step toward a complete understanding of neuronal zinc homeostasis.