Showing papers on "Zinc toxicity published in 2010"

Influence of pH and inorganic phosphate on toxicity of zinc to Arthrobacter sp. isolated from heavy-metal-contaminated sediments

Abstract: Because of its high solubility over a wide range of pH conditions, zinc is found in many natural and human-impacted systems. Zinc speciation is critical in assessing zinc toxicity to microorganisms because it varies considerably with pH and is dependent on other aqueous constituents. Combined results of thermodynamic modeling, statistical analysis, and batch culture studies using Arthrobacter sp. JM018 suggest that the toxic species may not be solely limited to the free ion, but also includes ZnHPO(4)(0)(aq). Cellular uptake of ZnHPO(4)(0)(aq) through the inorganic phosphate transporter (Pit family), which requires a neutral metal phosphate complex for phosphate transport, may explain the observed toxicity. Based on visual MINTEQ (v3.0) modeling, at 50 μM total zinc, ZnHPO(4)(0)(aq) constitutes 33, 70, and 76% of the neutral metal phosphate pool at pH 6, 7, and 8, respectively. At 50 μM total zinc, cultures supplied with organic phosphate (glycerol-3-phosphate) show no significant response to pH (p = 0.13) while inhibition of inorganic phosphate-supplemented cultures, whose neutral metal phosphates are increasingly dominated by ZnHPO(4)(0)(aq), show significant pH dependence (p = 9.45 × 10(-7)). Using sodium to decrease the distribution of ZnHPO(4)(0)(aq) in the neutral metal phosphate pool also decreased the pH dependent toxicity, further supporting this mechanism. These findings show the important role of minor zinc species in organism toxicity and have wider implications because the Pit inorganic phosphate transport system is widely distributed in Bacteria, Archaea, and Eukarya.

Light-induced photoreceptor and RPE degeneration involve zinc toxicity and are attenuated by pyruvate, nicotinamide, or cyclic light.

Abstract: Purpose Light-induced damage can be a problem after surgery or sun exposure. Short-duration, intense light causes preferential photoreceptor death in the superior central retina of albino mice and rats and serves as a model of oxidation-induced neurodegeneration. Previous work on retinal ischemia-induced neuronal death suggests the involvement of zinc (Zn2+) toxicity in the death and collapse of many retinal cell layers and demonstrates the protective efficacy of pyruvate. Retinal pigment epithelial (RPE) cells were shown to be sensitive to oxidative stress, and zinc, causing loss of nicotinamide adenine dinucleotide (NAD+) and adenine triphosphate (ATP), which was prevented by pyruvate and nicotinamide. We previously showed similar results in cortical neurons exposed to oxidative stress or Zn2+. In vivo, Zn2+ is normally present in the inner and outer segments (associated with rhodopsin), Bruch’s membrane and sclera (elastin), RPE, and the outer plexiform layer of the eye (synaptic). In this study, we examine the role of Zn2+ in oxidative stress and light-induced damage in vitro and in vivo.

Toxic effects of zinc on the development, growth, and survival of red sea bream Pagrus major embryos and larvae.

Abstract: This study investigated the zinc toxicity to red sea bream Pagrus major embryos and larvae at 18 ± 1°C (33 ± 1‰ in salinity) under laboratory conditions. The acute toxicity tests indicated that zinc 48-h LC50 to embryos and 96-h LC50 to larvae were 4.3 (3.3–6.3; 95% confidence limits) and 10.1 (9.0–11.4) mg l−1, respectively, suggesting that embryos were more sensitive than larvae to zinc exposure. The subchronic toxicity test, in which embryos and larvae were continuously exposed to 0, 0.1, 0.3, 0.5, 0.7, 1.0, 1.5, 2.0, and 2.5 mg Zn2+ l−1 solutions for 10 days, demonstrated that waterborne zinc had distinctly toxic effects on the development, growth, and survival of red sea bream embryos and larvae. Zinc exposure at concentrations ≥ 0.5 mg l−1 would lead to a low hatching rate (19–78%, vs. 98% in controls), high mortality (29–91%, vs. 10% in controls), and morphological abnormality (12–77%, vs. 0.3% in controls) in embryos and larvae, while it caused delay in time-to-hatch in embryos at concentrations ≥ 1.0 mg l−1. These four biological parameters were zinc concentration dependent and could be effective bioindicators for evaluating the toxicity of zinc to the early life stage of this fish. Heartbeats of embryos (9–13 beats 10 s−1) were relatively low and were not significantly influenced by zinc concentration, although they rose remarkably with elevated zinc concentration in larvae at the end of the test, particularly when it was ≥ 1.0 mg l−1 (36–38, vs. 31 beats 10 s−1 in controls). The total length (LT) of the larvae at the end of the test was reduced by 12.2% and 15.6% in the 1.0 and 2.0 mg l−1 solutions but did not vary significantly in other solutions in comparison with the controls. Heartbeat and LT were less sensitive to zinc exposure and might not be good biological parameters for determining the toxicity of zinc to the early life stage of red sea bream.

Tissue Plasminogen Activator Alters Intracellular Sequestration of Zinc through Interaction with the Transporter ZIP4

Abstract: Glutamatergic neurons contain free zinc packaged into neurotransmitter-loaded synaptic vesicles. Upon neuronal activation, the vesicular contents are released into the synaptic space, whereby the zinc modulates activity of postsynaptic neurons though interactions with receptors, transporters and exchangers. However, high extracellular concentrations of zinc trigger seizures and are neurotoxic if substantial amounts of zinc reenter the cells via ion channels and accumulate in the cytoplasm. Tissue plasminogen activator (tPA), a secreted serine protease, is also proepileptic and excitotoxic. However, tPA counters zinc toxicity by promoting zinc import back into the neurons in a sequestered form that is nontoxic. Here, we identify the zinc influx transporter, ZIP4, as the pathway through which tPA mediates the zinc uptake. We show that ZIP4 is upregulated after excitotoxin stimulation of the mouse, male and female, hippocampus. ZIP4 physically interacts with tPA, correlating with an increased intracellular zinc influx and lysosomal sequestration. Changes in prosurvival signals support the idea that this sequestration results in neuroprotection. These experiments identify a mechanism via which neurons use tPA to efficiently neutralize the toxic effects of excessive concentrations of free zinc.

Survivin mediates prostate cell protection by HIF‐1α against zinc toxicity

Abstract: BACKGROUND The prostate contains extremely high concentrations of zinc, but survives and grows without apparent injury. This begs the question as to how prostate cells avoid the toxic effects of zinc. In a previous study, the authors found that; HIF-1α is expressed concomitantly with the accumulation of zinc in the epithelial cells of normal rat prostates, the zinc ion stabilizes HIF-1α in prostate cells, and that HIF-1α protects prostate cells from zinc toxicity. In the present study, the authors addressed the mechanism responsible for the protective effect of HIF-1α in a high zinc environment. METHODS Immunofluorescent staining, immunoblotting, reverse transcription-polymerase chain reaction, reporter assay, and cell cycle analysis. RESULTS Survivin was induced by ZnCl2 in a HIF-1 dependent manner in both DU-145 and PNT2 prostate cells. Furthermore, HIF-1 induced survivin expression at the transcriptional level and the induction of survivin was abolished by HIF-1α knock-down. In addition, HIF-1-dependent survivin overexpression promoted prostrate cell survival and prevented cell arrest in the presence of high zinc concentrations, and si-survivin transfected cells under zinc rich conditions contained markedly higher levels of cleaved caspase-9 and PARP than si-con transfected cells. Finally, survivin expression patterns well matched rat prostate proliferation statuses. CONCLUSION Under zinc rich conditions, prostate epithelial cells HIF-1-dependently express survivin, which promotes prostate cell proliferation, and prevents apoptosis and cell cycle arrest. Accordingly, the HIF-1α-survivin pathway appears to facilitate prostate cell survival and growth in zinc rich environments, and this pathway could be a therapeutic target for the treatment of prostate hyperplasia. Prostate 70: 1179–1188, 2010. © 2010 Wiley-Liss, Inc.

Bioavailability of copper and zinc to poplar and microorganisms in a biosolids-amended soil

Abstract: The effects of high concentrations of copper (Cu) and zinc (Zn) in a soil treated with biosolids previously spiked with these metals on poplar (Populus deltoides × yunnanensis) were investigated in a pot trial. The total soil metal concentrations in the treatments were 12, 46, 137, and 226 mg Cu/kg and 25, 141, 433, and 686 mg Zn/kg. Copper accumulation was lower in poplar leaves than Zn and the maximum bioconcentration factor was 0.8 for Cu and 10 for Zn. Copper was not found to be toxic to plants at any level of application or to mycorrhiza up to 137 mg/kg, but it was found to be toxic to soil microorganisms at all levels of Cu addition. Copper application increased mycorrhiza colonisation up to 137 mg Cu/kg and root dry matter at 226 mg Cu/kg, but had no effect on leaf dry matter. Increasing Zn rate decreased all plant and soil parameters. Lower percentages of Cu in the soil exchangeable fraction, and a lower Cu2+ concentrations in soil solution relative to Zn indicated lower bioavailability of Cu. Dehydrogenase activity was reduced by 50% at total solution-phase Cu and Zn concentrations of 0.1 and 27 mg/L, respectively, and solid-phase exchangeable Cu and Zn concentrations of 5 and 169 mg/kg, respectively.

Zinc toxicity to aminergic neurotransmitters in rat brain.

Abstract: The present study was aimed to evaluate zinc toxicity to aminergic system in different areas of the brain of male albino rat, Rattus norvegicus. Zinc toxicity, evaluated as per Probit method was found to be 500 mg/kg body weight. For acute-dose studies, rats were given a single lethal dose of zinc chloride for one day only and for chronic-dose studies, the rats were administered with sub-lethal doses (1/10 th of lethal dose) of zinc chloride every day for 90 days continuously. Various constituents of the aminergic system viz. dopamine, norepinephrine, and epinephrine and the catabolizing enzyme, monoamine oxidase (MAO) were determined in different regions of rat brain such as olfactory lobe, hippocampus, cerebellum, and pons-medulla on selected time intervals/days under acute and chronic treatment with zinc. The results revealed that while the levels of all aminergic neurotransmitters were elevated differentially in the above mentioned areas of brain, MAO activity registered nonsignificant inhibition in all brain regions under zinc toxicity. All these changes in the aminergic system were subsequently manifested in the behavior of rat exhibiting the symptoms of mild tremors, reduced locomotor activity and emotions, restlessness followed by lacrymation, salivation, etc. From these observations, it was obvious that zinc treatment caused severe perturbations in the functions of the nervous system. Restoration of the aminergic system along with behavior to the near normal levels under chronic treatment indicates the onset of detoxification mechanisms or development of tolerance to zinc toxicity in the animal which was not probably so efficient under acute treatment.

Effects of zinc fertilization on the dynamics accumulation and distribution of dry matter and zinc in apple trees

Abstract: A sand culture experiment was conducted to study the dynamic accumulation and distribution of dry matter and zinc in organs of apple trees under three zinc application levels,Zn 0.013,0.254 and 5.07 mg/L.The results show that the growth and nutrient uptakes of apple trees are affected under both the deficiency and excess of Zn supplies.There are little effects on the accumulation and distribution of dry matter and nutrient under different zinc levels at the early growth stage,and the nutrients in roots and stems are utilized by branches and leaves for quickly growth.With the plant growth,the first peak of new roots turns up,the dry matter is accumulated quickly under different treatments,while the growth of roots is constrained by the deficiency and excess zinc supplies,and the zinc contents in each organs are significantly increased except branches and the order is Zn3 Zn2 Zn1.The dry matter accumulation is constrained by the deficiency and excess zinc supplies at the later growth stage,and zinc toxicity is happened under the excess zinc supply.The accumulation of zinc is increased quickly under the moderate and excess zinc supplies,however,the roots are increased under the deficiency treatment,and the distribution rate in root is significantly higher than that under the moderate and excess zinc supplies.These results indicates that at the later growth stage,the plant growth is constrained by the deficiency and excess zinc supplies;distribution rate of zinc in roots is higher than that in shoots under the lower zinc treatment,while the content of zinc in shoots is higher than that in roots under the moderate and excess zinc treatments.

Effect of zinc toxicity on the blood parameters of the laboratory mice

Abstract: The present search conducted at thecollegeofVeterinary Medicine–Universityof Basrahto investigate the effect of zinc toxicity on the physiological parameters, histopathological changes and reproductive efficiency in the laboratory mice. In this search, 32 mice were used, they were divided into two groups, each one consisted of four equal subgroups with 4 mice in each. The first three subgroups of each group were dosed via intraperitoneal injection with 60, 80 and 100 mg/kg zinc in the form of ZnSO 4 for 15 and 30 days. An equivalent volume of saline (0.9 %N.S) was administered to the fourth subgroup which was set as the control group. The investigation of blood parameters included RBC count, Hb concentration, PCV concentration, total and differential WBC count. The results here showed a significant decrease (P≤0.05) of RBC count, Hb concentration, PCV value, and neutrophil count, whereas there was a significant increase (P≤0.05) of total WBC count, lymphocyte count, monocyte count, and there were no significant differences in the acidophil count and basophil count.