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.

The zinc transporter Zip5 (Slc39a5) regulates intestinal zinc excretion and protects the pancreas against zinc toxicity.

Abstract: Background ZIP5 localizes to the baso-lateral membranes of intestinal enterocytes and pancreatic acinar cells and is internalized and degraded coordinately in these cell-types during periods of dietary zinc deficiency. These cell-types are thought to control zinc excretion from the body. The baso-lateral localization and zinc-regulation of ZIP5 in these cells are unique among the 14 members of the Slc39a family and suggest that ZIP5 plays a role in zinc excretion. Methods/Principal Findings We created mice with floxed Zip5 genes and deleted this gene in the entire mouse or specifically in enterocytes or acinar cells and then examined the effects on zinc homeostasis. We found that ZIP5 is not essential for growth and viability but total knockout of ZIP5 led to increased zinc in the liver in mice fed a zinc-adequate (ZnA) diet but impaired accumulation of pancreatic zinc in mice fed a zinc-excess (ZnE) diet. Loss-of-function of enterocyte ZIP5, in contrast, led to increased pancreatic zinc in mice fed a ZnA diet and increased abundance of intestinal Zip4 mRNA. Finally, loss-of-function of acinar cell ZIP5 modestly reduced pancreatic zinc in mice fed a ZnA diet but did not impair zinc uptake as measured by the rapid accumulation of 67zinc. Retention of pancreatic 67zinc was impaired in these mice but the absence of pancreatic ZIP5 sensitized them to zinc-induced pancreatitis and exacerbated the formation of large cytoplasmic vacuoles containing secretory protein in acinar cells. Conclusions These studies demonstrate that ZIP5 participates in the control of zinc excretion in mice. Specifically, they reveal a paramount function of intestinal ZIP5 in zinc excretion but suggest a role for pancreatic ZIP5 in zinc accumulation/retention in acinar cells. ZIP5 functions in acinar cells to protect against zinc-induced acute pancreatitis and attenuate the process of zymophagy. This suggests that it may play a role in autophagy.

Toxic effects of zinc on fathead minnows Pimephales promelas in soft water

Abstract: A fathead minnow life-cycle exposure to various zinc concentrations demonstrated that the most sensitive indicators of zinc toxicity were egg adhesiveness and fragility, which were significantly affected at 145 μg Zn 1−1 and above, but were not affected at 78 μg Zn 1−1 and below. These effects occurred shortly after the eggs were spawned (during water hardening) and therefore were not related to effects on the parental fish. Hatchability and survival of larvae were significantly reduced, and deformities at hatching were significantly increased at 295 ug Zn 1−1 and above. Acclimated and unacclimated groups of larvae exposed to identical zinc concentrations for 8 weeks after hatch showed only slight differences in sensitivity.

Effect of zinc toxicity on liver histology of Nile tilapia, Oreochromis niloticus

Abstract: In the present study the toxic effects of zinc (Zn) on the liver structure of Nile tilapia,Oreochromis niloticus were investigated. Additionally, we estimated whether Zn concentration and exposure period influence the degree and nature of histological changes in the liver of exposed fish. Two hundred and forty fish (the average weight was 24.30± 2.85 g) were distributed randomly in twenty four glass aquaria (80 L) with stocking density of 10 fish for each. The aquaria were divided into two groups: the first group was exposed to 2, 4 and 6 mg/L of ZnCl2 which represent 0.25, 0.50 and 0.75 of Zn LC50 respectively for one week (short exposure period); while the second group was exposed to the same concentrations of ZnCl2 with the same replicates for 4 weeks (long exposure period). In addition, control group were not exposed fish to ZnCl2 (0.00 LC50) were stocked with three replicates for each period. Fish mortality was significantly increased in a dose-dependent manner, without any significant effect of the exposure duration. Histological changes in the liver included hepatocyte degeneration, nuclear pycnosis, cellular swelling, and congestion of blood vessels. There was a marked difference in these changes among the different treatments of Zn concentrations in addition to the intensity of histological changes were however influenced by the extent of exposure period. Key words: Nile tilapia, Oreochromis niloticus, liver, histological changes, LC50 of Zinc.

Temperature, physiological time and zinc toxicity in the isopod Porcellio scaber.

Abstract: Temperature is an important controlling factor in the metabolism of ectotherms, and it may interact with the toxicity of heavy metals in a variety of ways. In this work, a study on the effect of different zinc concentrations (0.3, 13, 26, and 40 μmol/g dry litter) on growth (body weight) of the isopod Porcellio scaber was conducted using four temperature levels (12, 16, 20, and 24°C). The results demonstrated a significant effect for both zinc and temperature on the growth rate; the interaction between zinc and temperature was also significant. The Arrhenius function was used to describe the temperature–growth rate relationship, from which estimates for the activation energy were derived. A tendency for activation energy to decrease with increasing zinc concentration was observed. Isopods exposed to 13 μmol Zn/g had the highest activation energy and the highest growth rate. To analyze the effect of temperature on the internal body concentration of zinc, the exposure time was transformed into physiological time, calibrated at 15°C, for all experimental groups using the activation energies estimated earlier. The rate of zinc accumulation was derived from the relationship between internal body concentration and physiological exposure time. Differences between isopods cultured at different temperatures could be explained well by the effect of physiological exposure time. The interaction between temperature and zinc toxicity seems to be due not to increased accumulation of zinc at higher temperatures as such but to a physiological interaction with the energy metabolism.