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.

ZnT-1 extrudes zinc from mammalian cells functioning as a Zn2+/H+ exchanger

Abstract: ZnT-1 is a Cation Diffusion Facilitator (CDF) family protein, and is present throughout the phylogenetic tree from bacteria to humans. Since its original cloning in 1995, ZnT-1 has been considered to be the major Zn2+ extruding transporter, based on its ability to protect cells against zinc toxicity. However, experimental evidence for ZnT-1 induced Zn2+ extrusion was not convincing. In the present study, based on the 3D crystal structure of the ZnT-1 homologue, YiiP, that predicts a homodimer that utilizes the H+ electrochemical gradient to facilitate Zn2+ efflux, we demonstrate ZnT-1 dependent Zn2+ efflux from HEK 293T cells using FluoZin-3 and Fura 2 by single cell microscope based fluorescent imaging. ZnT-1 facilitates zinc efflux in a sodium-independent, pH-driven and calcium-sensitive manner. Moreover, substitution of two amino acids in the putative zinc binding domain of ZnT-1 led to nullification of Zn2+ efflux and rendered the mutated protein incapable of protecting cells against Zn2+ toxicity. Our results demonstrate that ZnT-1 extrudes zinc from mammalian cells by functioning as a Zn2+/H+ exchanger.

The Human Toxicity of Certain Trace Elements

Abstract: A review of the medical toxicology of cadmium, cobalt, selenium, arsenic, nickel, copper, manganese, tellurium, vanadium, molybdenum, zinc, and tin; emphasis is on industrial sources of in...

Zinc as an ambivalent but potent modulator of murine hair growth in vivo- preliminary observations.

Abstract: Oral zinc (Zn(2+)) is often employed for treating hair loss, even in the absence of zinc deficiency, although its mechanisms of action and efficacy are still obscure In the current study, we explored the in vivo effects of oral zinc using the C57BL/6 mouse model for hair research Specifically, we investigated whether continuous administration of high-dose ZnSO(4) x 7H(2)O (20 mg/ml) in drinking water affects hair follicle (HF) cycling, whether it retards or inhibits chemotherapy-induced alopecia (CIA) and whether it modulates the subsequent hair re-growth pattern Here, we show that high doses of oral zinc significantly inhibit hair growth by retardation of anagen development However, oral zinc also significantly retards and prolongs spontaneous, apoptosis-driven HF regression (catagen) Oral zinc can also retard, but not prevent, the onset of CIA in mice Interestingly, Zn(2+) treatment of cyclophosphamide-damaged HFs also significantly accelerates the re-growth of normally pigmented hair shafts, which reflects a promotion of HF recovery However, if given for a more extended time period, zinc actually retards hair re-growth Thus, high-dose oral zinc is a powerful, yet ambivalent hair growth modulator in mice, whose ultimate effects on the HF greatly depend on the timing and duration of zinc administration The current study also encourages one to explore whether oral zinc can mitigate chemotherapy-induced hair loss in humans and/or can stimulate hair re-growth

Acute Zinc Toxicity in Haemodialysis

Abstract: A country patient on home haemodialysis suffered acute nausea, vomiting, and fever during dialyses when she used water stored in a galvanized tank. She subsequently was found to have severe anaemia with raised plasma and erythrocyte zinc concentrations. Intercurrent hospital haemodialyses and subsequent home dialyses with deionized water were symptom-free. Experimental haemodialyses of dogs against small concentrations of zinc showed a disproportionate rise in plasma zinc and possible uptake of zinc by the liver.