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.

Hemin Through the Heme Oxygenase 1/Ferrous Iron, Carbon Monoxide System Involved in Zinc Tolerance in Oryza Sativa L.

Abstract: Several pharmacological experiments were performed to investigate the possible roles of heme oxygenase 1 (HO1) and its catalytic products on hemin-induced attenuation of excess zinc toxicity. The results showed that hemin markedly reduced concentrations of zinc in rice seedlings (including roots and shoots); this effect may be achieved by down-regulating the relative expression of OsZIP1, OsZIP3, OsZIP7, and OsZIP8. However, zinc protoporphyrin IX (Znpp, an HO1 inhibitor) application could reverse hemin-induced decreases in zinc accumulation and upregulate the relative expression of the above four genes. These results showed that HO1 is indeed involved in the mitigation of zinc stress. The following experiments were conducted to illustrate the contributive effect of different hemin by-products in the hemin-mediated attenuating effect. The results showed that bilirubin (BR) does not have any alleviative effect, whereas carbon monoxide (CO) has a similar effect as hemin; the alleviative effect of ferrous ion (Fe2+) is even better than that of hemin. Altogether, these findings suggested that hemin, through the HO1/Fe2+, CO system, may reduce zinc accumulation in rice seedlings and ultimately strengthen Zn tolerance of rice seedlings.

Zinc toxicity symptom development and partitioning of biomass and zinc in peanut plants 1

Abstract: High soil zinc (Zn) concentrations can cause Zn toxicity in peanuts (Arachis hypogaea L), which decreases productivity and can be fatal to the plants The objectives of this study were 1) to determine the optimal sampling time and plant part for diagnosis of Zn toxicity in peanuts, 2) to relate toxicity symptoms to plant Zn concentrations and calcium:zinc (Ca:Zn) ratios, and 3) to model the distribution of Zn and biomass into plant parts in relation to Zn concentration in the whole plant A greenhouse study utilized four soils (Lakeland sand, Tifton loamy sand, Greenville sandy clay loam, and Greenville sandy clay) with Zn applications of 0, 10, 20, and 40 mg Zn/kg soil Plants were sampled for analysis of nutrient concentrations, and Zn toxicity ratings were recorded biweekly Toxicity symptoms became visible 4–8 weeks after planting, with stunting appearing at four weeks, horizontal leaf growth and leaflet folding at six weeks, and stem splitting at eight weeks Optimal sampling time for diagn

Effects of chronic exposure to lead, copper, zinc, and cadmium on biomarkers of the European eel, Anguilla anguilla.

Abstract: Exposure to specific metallic compounds can cause severe deleterious modifications in organisms. Fishes are particularly prone to toxic effects from exposure to metallic compounds via their environment. Species that inhabit estuaries or freshwater environments can be chronically affected by persistent exposure to a large number of metallic compounds, particularly those released by industrial activities. In this study, we exposed yellow eels (European eel, Anguilla anguilla) for 28 days to environmentally relevant concentrations of four specific metals; lead (300, 600, and 1,200 μg/l), copper (40, 120, and 360 μg/l), zinc (30, 60, and 120 μg/l) and cadmium (50, 150, and 450 μg/l). The selected endpoints to assess the toxicological effects were neurotransmission (cholinesterasic activity in nervous tissue), antioxidant defense, and phase II metabolism (glutathione-S-transferase [GST] activity, in both gills and liver tissues), and peroxidative damage. The results showed an overall lack of effects on acetylcholinesterase for all tested metals. Lead, copper, and cadmium exposure caused a significant, dose-dependent, increase in GST activity in gill tissue. However, liver GST only significantly increased following zinc exposure. No statistically significant effects were observed for the thiobarbituric acid reactive substances assay, indicating the absence of peroxidative damage. These findings suggest that, despite the occurrence of an oxidative-based response after exposure to lead, copper, and cadmium, this had no consequence in terms of peroxidative membrane damage; furthermore, cholinergic neurotoxicity caused by lead, copper, and cadmium did not occur. The implications of these results are further discussed.