Electrochemical studies of organic compounds in zinc electrowinning circuits
- Authors: Vawdrey, Peter
- Date: 1986
- Type: Text , Thesis , Masters
- Full Text:
- Description: Most of Australia's zinc production is by the electrolytic zinc process, in which zinc is electrowon from an acid sulphate solution. The process is known to be exceptionally sensitive to the presence of trace impurities. At the Electrolytic Zinc plant (Risdon, Tasmania), isobenzofuranone (pthalide) has been detected in the electrowinning circuit, and found in higher concentrations during efficiency slumps. It was found that di-2-ethylhexyphthalate, (present in the liners and plastics used in the electrowinning circuit), is reduced to isobenzofuranone under the electrolysis conditions employed. In addition, an investigation involved a constant current electrolysis of a synthetic zinc electrolyte, as identified an additional pathway for the productionof isobenzofuranone. 2-Naphthol, added to the electrolysis circuit for current efficiency purposes, is also a major precursor of isobenzofuranone. 2-Napthol and possibly 1-nitroso-2-napthol can be oxidized to pthalic acid, either at a lead anode or via anode oxidation productions, and the phthalic acid produced can be reduced to isobenzofuranone at a zinc cathode. In addition, it was found that isobenzofurane is further reduced at the potential of zinc deposition to ultimately yield 2-methylbenzaldehyde. This compound, which has also been detected in Risdon plant electrolytes, is also toxic in the zince electrowinning circuit. The compound 2-methylabenzyl alcohol has also been detected via GLC examination of Risdon plant liquors. However, this compound was not detected in the present investigation, and thus no explanation can be offered for its presence in plant electrolytes. The toxicity of zinc electrolyte impurities on current efficiency was determined by a cyclic voltammetric technique. The results of this investigation indicate that the presence of isobenzofuranone and 2-methylbenzaldehyde can significantly lower current effciency, and the compounds phthalic acid and 2-methylbenzyl alcohol also lower efficiency.
- Description: Masters Degree in Applied Science
- Authors: Vawdrey, Peter
- Date: 1986
- Type: Text , Thesis , Masters
- Full Text:
- Description: Most of Australia's zinc production is by the electrolytic zinc process, in which zinc is electrowon from an acid sulphate solution. The process is known to be exceptionally sensitive to the presence of trace impurities. At the Electrolytic Zinc plant (Risdon, Tasmania), isobenzofuranone (pthalide) has been detected in the electrowinning circuit, and found in higher concentrations during efficiency slumps. It was found that di-2-ethylhexyphthalate, (present in the liners and plastics used in the electrowinning circuit), is reduced to isobenzofuranone under the electrolysis conditions employed. In addition, an investigation involved a constant current electrolysis of a synthetic zinc electrolyte, as identified an additional pathway for the productionof isobenzofuranone. 2-Naphthol, added to the electrolysis circuit for current efficiency purposes, is also a major precursor of isobenzofuranone. 2-Napthol and possibly 1-nitroso-2-napthol can be oxidized to pthalic acid, either at a lead anode or via anode oxidation productions, and the phthalic acid produced can be reduced to isobenzofuranone at a zinc cathode. In addition, it was found that isobenzofurane is further reduced at the potential of zinc deposition to ultimately yield 2-methylbenzaldehyde. This compound, which has also been detected in Risdon plant electrolytes, is also toxic in the zince electrowinning circuit. The compound 2-methylabenzyl alcohol has also been detected via GLC examination of Risdon plant liquors. However, this compound was not detected in the present investigation, and thus no explanation can be offered for its presence in plant electrolytes. The toxicity of zinc electrolyte impurities on current efficiency was determined by a cyclic voltammetric technique. The results of this investigation indicate that the presence of isobenzofuranone and 2-methylbenzaldehyde can significantly lower current effciency, and the compounds phthalic acid and 2-methylbenzyl alcohol also lower efficiency.
- Description: Masters Degree in Applied Science
The role of Zn2+ in insulin signalling and muscle atrophy
- Authors: Maier, Michelle
- Date: 2019
- Type: Text , Thesis , PhD
- Full Text:
- Description: Zn2+ is a broadly utilised ion in biology that has important catalytic, structural and regulatory roles within the cell. Zn2+ distribution in cells is maintained by zinc transporters, Zips and ZnTs, and disruptions in levels of Zn2+ have been associated with insulin resistance and muscle atrophy disorders. Zn2+ and reactive oxygen species (ROS) interact through inhibition of protein tyrosine phosphatases and ROS-mediated oxidation of the metal-binding metallothioneins (Mts) causing release of bound Zn2+, however the precise mechanisms are unclear. In the first study of this thesis addition of inhibitors of ROS-generating enzymes, superoxide dismutase 1 (SOD1) and NADPH oxidase 1 (NOX1) showed that only SOD1 inhibition increased short-term insulin-mediated Zn2+ release and increased the expression of Mt1 and 2. These results may suggest that ROS, in particular O2- accumulation through inhibition of SOD1, plays a role in insulin-mediated Zn2+ release. Inhibiting SOD1 prevents the conversion of O2- to H2O2 causing an accumulation of O2- in the cell which oxidises Mts to release Zn2+, thereby increasing Zn2+ levels within the cell. Manipulation of the expression of the zinc transporter Zip-7 has previously been shown to modulate cell signalling and glucose metabolism in C2C12 skeletal muscle cells, warranting further investigation into the role of Zn2+ within insulin signalling. Reducing Zip-7 expression when NOX1 was inhibited caused a decrease in Mt2 expression in response to insulin suggesting an interaction between insulin, Zip-7 and NOX1 activity but this requires further investigation. Skeletal muscle atrophy is a clinical symptom of insulin resistance and diabetes. Muscle atrophy is associated with increases in circulating glucocorticoid levels and accumulation of Zn2+ in muscle. This study investigates if Zn2+ homeostasis is disrupted in glucocorticoid-induced atrophy using C2C12 skeletal muscle cells treated with Dexamethasone (DEX) and iv insulin. Results demonstrate DEX-induced atrophy significantly increased the gene expression of the Mt1&2 and decreased glycogen accumulation when treated with insulin. Both confocal microscopy and flow cytometry showed significant increases in free cellular Zn2+ after DEX treatment. Notably, free Zn2+ levels observed with confocal microscopy increased after insulin treatment in control cells but decreased in DEX treated cells. Total cellular Zn2+ was increased by DEX treatment. This demonstrates that DEX causes Zn2+ accumulation in muscle cells and disrupts both Zn2+ homeostasis through blocking insulin-induced Zn2+ release, and insulin-induced glycogen synthesis. This raised the question of whether the same effects of atrophy on Zn2+ homeostasis apply to other cell systems. To investigate this, we examined adipose cells given that these too are involved in insulin resistance and muscle atrophy disorders. In this study we found similar increases in mRNA abundance of Mt1 & 2. Confocal microscopy revealed that DEX treatment caused changes in the distribution of free Zn2+ within peri-nuclear and cytosolic regions of the cell upon stimulation with insulin. Furthermore, investigation into morphometric changes using Oil Red O staining and particle analysis through Coherent Anti-Stokes Ramen Spectrophotometry (CARS) microscopy showed changes in cell and lipid droplet size consistent with reduced lipid turnover in DEX treated cells. These results highlight a potential mechanistic role for Zn2+ in the development of atrophy in 3T3-L1 adipocytes where increased free Zn2+ and its redistribution in cells may inhibit lipid metabolism downstream of insulin signalling. These findings show that insulin-induced Zn2+ release is disrupted by glucocorticoids and this is associated with insulin resistance. Restoring control of Zn2+ homeostasis, possibly through controlling oxidation or manipulating Zn2+ levels directly, may prove beneficial in metabolic disease states such as diabetes.
- Description: Doctor of Philosophy
- Authors: Maier, Michelle
- Date: 2019
- Type: Text , Thesis , PhD
- Full Text:
- Description: Zn2+ is a broadly utilised ion in biology that has important catalytic, structural and regulatory roles within the cell. Zn2+ distribution in cells is maintained by zinc transporters, Zips and ZnTs, and disruptions in levels of Zn2+ have been associated with insulin resistance and muscle atrophy disorders. Zn2+ and reactive oxygen species (ROS) interact through inhibition of protein tyrosine phosphatases and ROS-mediated oxidation of the metal-binding metallothioneins (Mts) causing release of bound Zn2+, however the precise mechanisms are unclear. In the first study of this thesis addition of inhibitors of ROS-generating enzymes, superoxide dismutase 1 (SOD1) and NADPH oxidase 1 (NOX1) showed that only SOD1 inhibition increased short-term insulin-mediated Zn2+ release and increased the expression of Mt1 and 2. These results may suggest that ROS, in particular O2- accumulation through inhibition of SOD1, plays a role in insulin-mediated Zn2+ release. Inhibiting SOD1 prevents the conversion of O2- to H2O2 causing an accumulation of O2- in the cell which oxidises Mts to release Zn2+, thereby increasing Zn2+ levels within the cell. Manipulation of the expression of the zinc transporter Zip-7 has previously been shown to modulate cell signalling and glucose metabolism in C2C12 skeletal muscle cells, warranting further investigation into the role of Zn2+ within insulin signalling. Reducing Zip-7 expression when NOX1 was inhibited caused a decrease in Mt2 expression in response to insulin suggesting an interaction between insulin, Zip-7 and NOX1 activity but this requires further investigation. Skeletal muscle atrophy is a clinical symptom of insulin resistance and diabetes. Muscle atrophy is associated with increases in circulating glucocorticoid levels and accumulation of Zn2+ in muscle. This study investigates if Zn2+ homeostasis is disrupted in glucocorticoid-induced atrophy using C2C12 skeletal muscle cells treated with Dexamethasone (DEX) and iv insulin. Results demonstrate DEX-induced atrophy significantly increased the gene expression of the Mt1&2 and decreased glycogen accumulation when treated with insulin. Both confocal microscopy and flow cytometry showed significant increases in free cellular Zn2+ after DEX treatment. Notably, free Zn2+ levels observed with confocal microscopy increased after insulin treatment in control cells but decreased in DEX treated cells. Total cellular Zn2+ was increased by DEX treatment. This demonstrates that DEX causes Zn2+ accumulation in muscle cells and disrupts both Zn2+ homeostasis through blocking insulin-induced Zn2+ release, and insulin-induced glycogen synthesis. This raised the question of whether the same effects of atrophy on Zn2+ homeostasis apply to other cell systems. To investigate this, we examined adipose cells given that these too are involved in insulin resistance and muscle atrophy disorders. In this study we found similar increases in mRNA abundance of Mt1 & 2. Confocal microscopy revealed that DEX treatment caused changes in the distribution of free Zn2+ within peri-nuclear and cytosolic regions of the cell upon stimulation with insulin. Furthermore, investigation into morphometric changes using Oil Red O staining and particle analysis through Coherent Anti-Stokes Ramen Spectrophotometry (CARS) microscopy showed changes in cell and lipid droplet size consistent with reduced lipid turnover in DEX treated cells. These results highlight a potential mechanistic role for Zn2+ in the development of atrophy in 3T3-L1 adipocytes where increased free Zn2+ and its redistribution in cells may inhibit lipid metabolism downstream of insulin signalling. These findings show that insulin-induced Zn2+ release is disrupted by glucocorticoids and this is associated with insulin resistance. Restoring control of Zn2+ homeostasis, possibly through controlling oxidation or manipulating Zn2+ levels directly, may prove beneficial in metabolic disease states such as diabetes.
- Description: Doctor of Philosophy
- «
- ‹
- 1
- ›
- »