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PubMed1994

Effect of zinc-chelating dipeptides on osteoblastic MC3T3-E1 cells: activation of aminoacyl-tRNA synthetase.

The effect of zinc-chelating dipeptides on osteoblastic MC3T3-E1 cells was investigated. As zinc compounds, we used zinc sulfate, AHZ, di(N-acetyl-beta-alanyl-L-histidinato)zinc (AAHZ), and di(histidino)zinc (HZ). Cells were cultured for 72 h in the presence of zinc compounds (10(-8)-10(-5) M). The effect of AHZ (10(-7) and 10(-6) M) to increase protein and deoxyribonucleic acid (DNA) contents in the cells was the greatest in comparison with those of other zinc compounds. Zinc sulfate and HZ at 10(-7) M did not have an effect on the cellular protein content. AHZ (10(-6) M) had a potent effect on cell proliferation, although zinc sulfate (10(-6) M) had no effect. beta-Alanyl-L-histidine (10(-6) and 10(-5) M) did not have an appreciable effect on the cells. Those effects of AHZ (10(-6) M) on osteoblastic cells were completely abolished by the presence of cycloheximide (10(-6) M). AHZ (10(-8)-10(-5) M) directly activated [3H]leucyl-tRNA synthetase in the cell homogenate, whereas the effect of zinc sulfate was seen at 10(-6) and 10(-5) M. The present study suggests that the chemical form of zinc-chelating beta-alanyl-L-histidine (AHZ) can reveal a potent anabolic effect on osteoblastic cells, and that AHZ directly stimulates protein synthesis.

3T3 Cells↗
PubMed1996

Stimulatory effect of zinc-chelating dipeptide on deoxyribonucleic acid synthesis in osteoblastic MC3T3-E1 cells.

Whether deoxyribonucleic acid (DNA) synthesis in osteoblastic MC3T3-E1 cells is stimulated by zinc, an activator of bone formation, was investigated in vitro. After subculture for 3 days, the cells were cultured for up to 3 days (72 h) with zinc sulfate or zinc-chelated dipeptide (beta-alanyl-L-histidinato zinc; AHZ) in the range of 10(-7) to 10(-5) M. The culture with zinc compounds (10(-5) M) produced a significant increase of cell number, DNA content, and protein concentration in the cells, as reported previously. The culture with zinc compounds (10(-6) and 10(-5) M) clearly stimulated DNA synthesis in the homogenate, when it was estimated by the incorporation of [3H]deoxythymidine 5'-triphosphate into the DNA in the homogenate of cells. The AHZ effect was greater than that of zinc sulfate. The culture together with cycloheximide (19(-6) M) completely abolished the zinc compounds (10(-5) M)-induced increase of DNA synthesis in the cells, suggesting that the zinc compound effect is based on a newly synthesized protein component. Moreover, when zinc sulfate (10(-7) and 10(-6) M) or AHZ (10(-8) to 10(-5) M) was added into the reaction mixture with the homogenate of cells cultured without zinc compounds, the DNA synthesis was clearly increased. The effect of addition of zinc compounds (10(-6) M) on the DNA synthesis was completely inhibited by the presence of staurosporine (10(-8) M), an inhibitor of protein kinase C, or okadaic acid (10(-7) M), an inhibitor of protein phosphatase. The present study demonstrates that zinc compounds have a stimulatory effect on DNA synthesis in osteoblastic cells.

Animals↗
PubMedDate not supplied

Thermal degradation processes of end-capped poly(L-lactide)s in the presence and absence of residual zinc catalyst.

Thermal degradation processes of end-capped poly(L-lactide)s (PLLAs) were investigated by means of several thermoanalytical techniques under both isothermal and nonisothermal conditions. Based on the thermogravimetric analysis, it was found that two distinct processes at temperatures below and above 330 degrees C were existed in the nonisothermal degradation for PLLA samples depending on the amounts of residual zinc compounds from synthesis process. Isothermal degradation experiments at different temperature regions showed that the sample weight of PLLA decreased linearly with time in both cases, whereas the changes in molecular weight revealed different tendency for the temperature. On the basis of characterization of the residual PLLA molecules after isothermal degradation at 330 degrees C, it was confirmed that the omega chain end of the residual molecules was an acrylic ester unit. Majority of volatile products during thermal degradation of PLLA was the lactide regardless of the degradation temperature. From these results, it is concluded that, during the thermal degradation of PLLA samples in the presence of large amounts of residual zinc compounds, the zinc compounds catalyze both the intermolecular transesterification generating PLLA with low molecular weights and the selective unzipping depolymerization of PLLA with low molecular weights at temperatures below 330 degrees C. In contrast, the primary reaction of thermal degradation for PLLA in the absence of residual zinc compounds above 330 degrees C is a competition between the random chain scission via a cis-elimination reaction and the cyclic rupture via intramolecular transesterification of PLLA molecules. In addition, it was evidenced that the racemization of lactic acid units in the main chain of PLLA molecules occurred at temperatures above 330 degrees C.

Catalysis↗
PubMed2006

Antiproliferative and apoptotic effects of zinc-citrate compound (CIZAR(R)) on human epithelial ovarian cancer cell line, OVCAR-3.

OBJECTIVE: Zinc inhibits the growth of several carcinoma cells through induction of cell cycle arrest and apoptosis. The intracellular concentration of zinc and its dynamic changes are critically important in cell biology. We investigated the effects of zinc-citrate compound (CIZAR) on normal human ovarian epithelial cells (NOSE) and human epithelial ovarian cancer cell line, OVCAR-3. METHODS: To investigate the potential effect of CIZAR on cell growth and survival, cells were treated with different doses and exposed to different times. Intracellular concentration of zinc was measured by colorimetric assay. Mitochondrial aconitase activity was determined in cell extracts using aconitase assay. The flow cytometric assay, DNA laddering, and morphological analysis were done to investigate cytotoxic effects of CIZAR. Molecular mechanism of cell death was investigated by p53, Bcl-xL, Bcl-2, Bax protein, activity of caspase-3 and -12, and activity of telomerase. RESULTS: CIZAR-induced zinc accumulation in OVCAR-3 cells was higher than that in NOSE cells. CIZAR(R) treatment resulted in a time- and dose-dependent decrease in cell number in OVCAR-3 cells in comparison with NOSE cells. M-aconitase activity was significantly decreased in OVCAR-3 cells within 4 h exposure to CIZAR but relatively constant in NOSE cells. The flow cytometric assay, DNA laddering, and morphological analysis indicated apoptosis in OVCAR-3 cells but not in NOSE cells. CIZAR increased the expression of p21(waf1) which is a part of p53-independent pathway and induced reduction of telomerase activity. CIZAR reduced expression of Bcl-2 and Bcl-xL proteins but induced expression of Bax protein. CIZAR induced apoptosis of OVCAR-3 cells by activation of caspase-12 and caspase-3 pathway. CONCLUSIONS: Exposure to CIZAR induces apoptosis in OVCAR-3 cells which accumulate high intracellular levels of zinc, but not in NOSE cells, which do not accumulate high levels of zinc. CIZAR(R) prevents the proliferation of OVCAR-3 cells by inactivation of m-aconitase activity and induces apoptosis by induction of proapoptotic gene (Bax), repression of antiapoptotic genes (Bcl-2, Bcl-xL), and consequently activation of caspase-3. CIZAR also induced activation of caspase-12. The CIZAR will offer new window in prevention and treatment of epithelial ovarian cancer.

Aconitate Hydratase↗
PubMed2006

Cytotoxic effect of zinc-citrate compound on choriocarcinoma cell lines.

This study investigated the cytotoxic effect of zinc-citrate compound (CIZAR) on choriocarcinoma cell lines. Primary cultured normal trophoblast cells (NPT), human tumorigenic poorly differentiated trophoblast cell line (HT), and choriocarcinoma cell line (BeWo) were exposed to different concentrations of CIZAR and cultured at different times. Cell viability was determined by CCK-8 assay. The effects on cell cycle progression, population distribution and apoptotic incidence were determined by flow cytometry. The appearance of apoptosis was confirmed by DNA laddering and DAPI staining. The quantitative analysis of telomerase was measured by TRAPeze telomerase detection kit. The molecular mechanism of CIZAR-induced apoptosis was examined with Western blot analysis and colorimetric caspase-3 activity assay. In in vitro condition, CIZAR had a selective cytotoxic effect on choriocarcinoma cell line in dose- and time-dependent patterns. Flow cytometric analysis, DNA laddering, and DAPI staining indicated that BeWo cells only have been induced apoptosis by CIZAR. Shortening of telomere was also observed only in BeWo cells. Results also displayed that CIZAR-induced apoptosis involves the up-regulation of p21(WAF1) and Bax protein and down-regulation of Bcl-2 which were accompanied by the activation of caspase-3. Taken together, our results suggest that CIZAR is an apoptotic inducer in malignant trophoblast cells (BeWo).

Apoptosis↗
PubMed1999

Na2Zn3(CO3)4.3H2O: a potentially useful compound for zinc supplementation.

The infrared and Raman spectra of the title compound were recorded and are briefly discussed on the basis of its structural characteristics. Its thermal behaviour was investigated by means of TG and DTA measurements. Several dissolution tests were also performed. The results support the potential usefulness of this double carbonate as a useful compound for Zn(II) supplementation.

Animals↗
PubMed1997

Characterization of zinc effect to inhibit osteoclast-like cell formation in mouse marrow culture: interaction with dexamethasone.

The inhibitory effect of zinc compounds on osteoclast-like cell formation in mouse marrow culture in vitro was characterized. The bone marrow cells were cultured for 7 days in alpha-minimal essential medium containing a well-known bone resorbing agent, 1,25-dihydroxyvitamin D3[1,25(OH)2D3] or prostaglandin E2 (PGE2). Osteoclast-like cell formation was estimated by staining for tartrate-resistant acid phosphatase (TRACP), a marker enzyme of osteoclasts. The presence of 1,25(OH)2D3 (10(-8) M) or PGE2 (10(-6) M) induced a remarkable increase in osteoclast-like multinucleated cells. These increases were enhanced by the presence of dexamethasone (10(-9) to 10(-6) M). The dexamethasone (10(-7) M)-enhanced osteoclast-like cell formation was not inhibited by the presence of zinc sulfate (10(-6) M) or zinc-chelating dipeptide (beta-alanyl-L-histidinato zinc; 10(-6) M), although the zinc compounds had an inhibitory effect on osteoclastic formation in the absence of the steroid. The effect of dexamethasone was not seen, when the steroid was added at the later stage of culture with bone-resorbing agents. In this case, the inhibitory effect of zinc compounds was clearly revealed. This effect of zinc compounds disappeared in the presence of Ca2+-chelating agent (0.5 mM EGTA). The present study suggests that zinc compounds have an inhibitory effect at the stage of differentiation of preosteoclastic cells in bone marrow cell culture system.

Animals↗
PubMedDate not supplied

The influence of zinc on apoptosis.

This review summarizes the evidence that apoptosis is modulated by intracellular excess or deficiency of Zn2+, considers mechanisms whereby Zn2+ may influence apoptosis, and delineates gaps in current knowledge and opportunities for research. The experimental evidence supports four major conclusions: [1] Zinc deficiency, resulting from dietary deprivation of mice, or exposure of cultured cells to membrane-permeable Zn(2+)-chelators, can induce apoptosis; [2] Zinc supplementation, either by pretreating mice with ZnSO4, or adding Zn2+ to the media of cell cultures, can prevent apoptotic death. Zn2+ protects against the apoptosis induced by diverse physical, chemical, or immunologic stimuli in cultured cells of lymphoid, hepatic, or neoplastic origin; [3] Zn2+ does not affect the triggering events or earliest signs of apoptosis, but acts later in the apoptotic pathway, preventing endonucleosomal fragmentation and subsequent cytolysis; and [4] An intracellular pool of chelatable Zn2+ plays a critical role in apoptosis, possibly by modulating the activation or activity of endonuclease(s). These conclusions should alert pharmacologists and physicians to the potential therapeutic applications of zinc compounds and zinc chelators in clinical disorders and diseases that involve apoptosis, and to the relevance of zinc nutrition in such conditions.

Animals↗
PubMed1993

[Lowering the acute toxicity of ethanol with a zinc-metallothionein compound].

The homogeneous drug of zinc-metallothionein (zinc-MT) which characterized according to the molecular weight and UV-absorption spectra was obtained from the liver of the rats preliminary injected with the zinc chloride. It was shown that zinc-MT (0.5-4 mg/kg of protein) injected to the mouse 10 min before the ethanol decrease the acute toxicity of the alcohol. The preliminary injection of the control mixture consisted the albumin, cysteine and zinc chloride in proportions and dose corresponding to the dose 3 mg/kg of zinc-MT did not change LD50 of ethanol. The possible mechanism of the effect is discussed. The most possible is the stabilization of the lipid peroxidation in the liver or the restoration of the thiol groups pool at the alcohol intoxication by the zinc-MT.

Animals↗
PubMed2002

Hydrolysis of natural and artificial phosphoesters using zinc model compound with a histidine-containing pseudopeptide.

Zinc(II) complex with histidine-containing pseudopeptide derived from N,N'-bis(benzylhistidyl) diethylenetriamine L was examined as catalyst for the hydrolysis of bis(p-nitrophenyl) phosphate (BNPP), p-nitrophenyl phosphate (NPP), adenylyl-(3'-5')adenosine (ApA), thymidylyl-(3'-5') thymidine (TpT) and PBR 322 supercoiled DNA. The stepwise protonation constants of the ligand, stability constants for its zinc(II) complex LZn have been determined potentiometrically in aqueous solution. LZn efficiently hydrolyzed BNPP and NPP and their pseudo-first-order rate constants k(obs) are 1.1 x 10(-5) s(-1) and 2.1 x 10(-5) s(-1), respectively. Bell-shaped pH-k(obs) profile was seen in BNPP hydrolysis around pH 7. Kinetic parameters were obtained from temperature dependence of hydrolysis rate constants where entropy of activation showed considerably high negative value. ApA and TpT as RNA-type and DNA-type dinucleotides were slowly hydrolyzed by LZn. On the basis of the kinetic evidence of bell-shaped pH-k(obs) profile and species distribution curve, we propose a mechanism for LZn-promoted hydrolysis of BNPP as well as ApA where cooperative achieve of zinc-hydroxo and zinc-aqua complex species may be responsible for enzymatic activity. The agarose gel electrophoresis and AFM demonstrated that LZn performed good activity on the selective cleavage of pBR322 supercoiled DNA at pH 7.0 providing evidence for its probable applicability.

Histidine↗
PubMed1995

Inhibitory effect of zinc-chelating dipeptide on parathyroid hormone-stimulated osteoclast-like cell formation in mouse marrow cultures: involvement of calcium signaling.

A possible mechanism of zinc action inhibiting the PTH-induced osteoclast-like cell formation in mouse marrow culture system in vitro was investigated. Bone marrow cells were cultured for 7 days in alpha-minimal essential medium containing a well-known bone-resorbing agent parathyroid hormone (1-34) (PTH). Osteoclast-like cell formation was estimated with staining for tartrate-resistant acid phosphatase (TRACP), a marker enzyme of osteoclasts. The effect of zinc sulfate (10(-6) M) or beta-alanyl-L-histidinato zinc (AHZ; 10(-6) M) inhibiting the PTH (10(-8) M)-induced osteoclast-like cell formation was clearly seen in the absence or presence of theophylline (10(-4) M). However, zinc compounds did not inhibit the stimulatory effect of dibutyryladenosine 3',5'-cyclic monophosphate (DBcAMP; 10(-4) M) on osteoclast-like cell formation. The stimulating effect of PTH (10(-8) M) on osteoclast-like cell formation was clearly weakened (about 50%) in the presence of EGTA (1.0 mM) or dibucaine (10(-5) M). Phorbol 12-myristate 13-acetate (PMA), a protein kinase C activator (10(-8) to 10(-6) M), clearly stimulated osteoclast-like cell formation. PMA effect was inhibited by the presence of AHZ (10(-6) M) or zinc sulfate (10(-8) M). However, the inhibitory effect of zinc compounds was not seen in the presence of both PTH (10(-8) M) and PMA (10(-6) M). The present findings suggest that zinc compounds inhibit PTH-stimulated osteoclast-like cell formation mediated through the Ca(2+)-dependent activation of protein kinase C.

Animals↗
PubMed1989

Extended X-ray absorption fine structure (EXAFS) investigations of model compounds for zinc enzymes.

A test of the ability of extended X-ray absorption fine structure (EXAFS) to determine structural information with specific reference to zinc sites in enzymes has been made. X-ray absorption spectra of 18 compounds of zinc have been measured and the nearest-neighbour scattering has been interpreted using a Fourier transform and an ab initio technique. Empirical Zn-N, Zn-O, Zn-S and Zn-Cl amplitude and phase functions have been extracted from Zn(C3H4N2)4(ClO4)2, ZnO, Zn(S2COC2H5)2 and [N(CH3)4]2[ZnCl4], respectively and tabulated as a function of the wavevector with respect to 9660.0 eV X-ray energy. These amplitude and phase functions were then tested with respect to the other 14 compounds. For a single species of atoms in the first coordination shell the interatomic distances can be established to +/- 0.5 pm (+/- 5 x 10(-3) A) whilst when mixed shells exist errors in distances are +/-4 pm (+/- 40 x 10(-3) A). Coordination numbers are given to +/- 16% for the single species case a and +/- 25% for the mixed coordination case. Using the theoretical amplitude and phase functions of McKale et al. [(1988) J. Am. Chem. Soc. 110, 3763-3768] the deduced distances are systematically too small by an average of 0.6 pm (6 x 10(-3) A). The errors in the coordination numbers are 18%.

Enzymes↗
PubMed1997

Zinc enhancement of 17beta-estradiol's anabolic effect in osteoblastic MC3T3-E1 cells.

The anabolic effect of 17beta-estradiol in osteoblastic MC3T3-E1 cells was investigated. The cells were cultured for 3 days in the medium containing either vehicle or 17beta-estradiol (10(-11)-10(-9) M). 17beta-Estradiol significantly increased alkaline phosphatase activity and protein concentration in the cells. The steroid (10(-9) M) also significantly elevated the cell numbers and the cellular DNA content. The anabolic effect by 17beta-estradiol was blocked by the presence of dipicolinate (10(-3) M), a chelator of zinc ion, suggesting a role of cellular zinc in osteoblastic cell function. The presence of zinc sulfate (10(-5) M) or beta-alanyl-L-histidinato zinc (AHZ) (10(-5) M) significantly enhanced the 17beta-estradiol (10(-10) or 10(-9) M)-induced increase of alkaline phosphatase activity and protein concentration in the cells; the effect of AHZ was greater than that of zinc sulfate. The enhancement by zinc compounds was not based on the augmentation of osteoblastic cell numbers. The co-addition of cycloheximide (10(-6) M), an inhibitor of protein synthesis, completely blocked the zinc compound (10(-5) M)-induced enhancement of 17beta-estradiol's (10(-9) M) effect to increase alkaline phosphatase activity and protein concentration in the cells. Moreover, the anabolic effect of 17beta-estradiol together with or without zinc compounds was abolished by the presence of staurosporine (10(-8) M), an inhibitor of protein kinase C, or of okadaic acid (10(-7) M), an inhibitor of protein phosphatase. The present study demonstrates that the anabolic effect of 17beta-estradiol is enhanced by zinc-chelating dipeptide in osteoblastic MC3T3-E1 cells, and that the enhancing effect may involve protein synthesis and protein kinase activity.

3T3 Cells↗
PubMed1999

Zinc.

The use of zinc in metal alloys and medicinal lotions dates back before the time of Christ. Currently, most of the commercial production of zinc involves the galvanizing of iron and the manufacture of brass. Some studies support the use of zinc gluconate lozenges to treat the common cold, but there are insufficient data at this time to recommend the routine use of these lozenges. Zinc is an essential co-factor in a variety of cellular processes including DNA synthesis, behavioral responses, reproduction, bone formation, growth, and wound healing. Zinc is a relatively common metal with an average concentration of 50 mg/kg soil and a range of 10-300 mg/kg soil. Meat, seafood, dairy products, nuts, legumes, and whole grains contain relatively high concentrations of zinc. The mobility of zinc in anaerobic environments is poor and therefore severe zinc contamination occurs primarily near points sources of zinc release. The recommended daily allowance for adults is 15 mg zinc. The ingestion of 1-2 g zinc sulfate produces emesis. Zinc compounds can produce irritation and corrosion of the gastrointestinal tract, along with acute renal tubular necrosis and interstitial nephritis. Inhalation of high concentrations of zinc chloride from smoke bombs detonated in closed spaces may cause chemical pneumonitis and adult respiratory distress syndrome. In the occupational setting inhalation of fumes from zinc oxide is the most common cause of metal fume fever (fatigue, chills, fever, myalgias, cough, dyspnea, leukocytosis, thirst, metallic taste, salivation). Zinc compounds are not suspected carcinogens. Treatment of zinc toxicity is supportive. Calcium disodium ethylenediaminetetraacetate (CaNa2EDTA) is the chelator of choice based on case reports that demonstrate normalization of zinc concentrations, but there are few clinical data to confirm the efficacy of this agent.

Animals↗
PubMed2004

Interaction of selenium compounds with zinc finger proteins involved in DNA repair.

As an essential element, selenium is present in enzymes from several families, including glutathione peroxidases, and is thought to exert anticarcinogenic properties. A remarkable feature of selenium consists of its ability to oxidize thiols under reducing conditions. Thus, one mode of action recently suggested is the oxidation of thiol groups of metallothionein, thereby providing zinc for essential reactions. However, tetrahedral zinc ion complexation to four thiolates, similar to that found in metallothionein, is present in one of the major classes of transcription factors and other so-called zinc finger proteins. Within this study we investigated the effect of selenium compounds on the activity of the formamidopyrimidine-DNA glycosylase (Fpg), a zinc finger protein involved in base excision repair, and on the DNA-binding capacity and integrity of xeroderma pigmentosum group A protein (XPA), a zinc finger protein essential for nucleotide excision repair. The reducible selenium compounds phenylseleninic acid, phenylselenyl chloride, selenocystine, ebselen, and 2-nitrophenylselenocyanate caused a concentration-dependent decrease of Fpg activity, while no inhibition was detected with fully reduced selenomethionine, methylselenocysteine or some sulfur-containing analogs. Furthermore, reducible selenium compounds interfered with XPA-DNA binding and released zinc from the zinc finger motif, XPAzf. Zinc release was even evident at high glutathione/oxidised glutathine ratios prevailing under cellular conditions. Finally, comparative studies with metallothionein and XPAzf revealed similar or even accelerated zinc release from XPAzf. Altogether, the results indicate that zinc finger motifs are highly reactive towards oxidizing selenium compounds. This could affect gene expression, DNA repair and, thus, genomic stability.

Animals↗
PubMed2006

Trichomes of tobacco excrete zinc as zinc-substituted calcium carbonate and other zinc-containing compounds.

Tobacco (Nicotiana tabacum L. cv Xanthi) plants were exposed to toxic levels of zinc (Zn). Zn exposure resulted in toxicity signs in plants, and these damages were partly reduced by a calcium (Ca) supplement. Confocal imaging of intracellular Zn using Zinquin showed that Zn was preferentially accumulated in trichomes. Exposure to Zn and Zn + Ca increased the trichome density and induced the production of Ca/Zn mineral grains on the head cells of trichomes. These grains were aggregates of submicrometer-sized crystals and poorly crystalline material and contained Ca as major element, along with subordinate amounts of Zn, manganese, potassium, chlorine, phosphorus, silicon, and magnesium. Micro x-ray diffraction revealed that the large majority of the grains were composed essentially of metal-substituted calcite (CaCO3). CaCO3 polymorphs (aragonite and vaterite) and CaC2O4 (Ca oxalate) mono- and dihydrate also were identified, either as an admixture to calcite or in separate grains. Some grains did not diffract, although they contained Ca, suggesting the presence of amorphous form of Ca. The presence of Zn-substituted calcite was confirmed by Zn K-edge micro-extended x-ray absorption fine structure spectroscopy. Zn bound to organic compounds and Zn-containing silica and phosphate were also identified by this technique. The proportion of Zn-substituted calcite relative to the other species increased with Ca exposure. The production of Zn-containing biogenic calcite and other Zn compounds through the trichomes is a novel mechanism involved in Zn detoxification. This study illustrates the potential of laterally resolved x-ray synchrotron radiation techniques to study biomineralization and metal homeostasis processes in plants.

Calcium Carbonate↗
PubMed2006

Sulfidation of zinc plating sludge with Na2S for zinc resource recovery.

A high amount of zinc disposed in the landfill sites as a mixed-metal plating sludge represents a valuable zinc source. To recover zinc from the plating sludge, a sulfidation treatment is proposed in this study, while it is assumed that ZnS formed could be separated by flotation. The sulfidation treatment was conducted by contacting simulated zinc plating sludge with Na(2)S solution at S(2-) to Zn(2+) molar ratio of 1.5 for a period of 1-48 h, while changing the solid to liquid (S:L) ratio from 0.25:50 to 1.00:50. The conversion of zinc compounds to ZnS was determined based on the consumption of sulfide ions. The reaction products formed by the sulfidation of zinc were identified by X-ray diffraction (XRD). As a result, it was found that the conversion of zinc compounds to ZnS increased with an increase in S:L ratio. A maximum conversion of 0.809 was obtained at an S:L ratio of 1.00:50 after 48 h. However, when the zinc sludge treated at S:L ratio of 1.00:50 for 48 h was subjected to XRD analyses, only ZnS was identified in the treated zinc sludge. The result suggested that the rest of zinc sludge remained unreacted inside the agglomerates of ZnS. The formation behavior of ZnS was predicted by Elovich equation, which was found to describe the system satisfactorily indicating the heterogeneous nature of the sludge.

Electroplating↗