ZINC ACETATE

ZINC ACETATE

CAS No. : 557-34-6/5970-45-6
EC No. : 209-170-2

Zinc Acetate

Zinc acetate is a salt with the formula Zn(CH3CO2)2, which commonly occurs as the dihydrate Zn(CH3CO2)2·2H2O. Both the hydrate and the anhydrous forms are colorless solids that are commonly used in chemical synthesis and as dietary supplements. Zinc acetates are prepared by the action of acetic acid on zinc carbonate or zinc metal. When used as a food additive, it has the E number E650.

Uses
Dietary and medicinal applications
Zinc acetate has been used in lozenges for treating the common cold. Zinc acetate can also be used to treat zinc deficiencies.[2] As an oral daily supplement it is used to inhibit the body's absorption of copper as part of the treatment for Wilson's disease.[3] Zinc acetate is also sold as an astringent in the form of an ointment, a topical lotion, or combined with an antibiotic such as erythromycin for the topical treatment of acne.[4] It is commonly sold as a topical anti-itch ointment.

Industrial applications
Industrial applications include wood preservation, manufacturing other zinc salts, polymers, manufacture of ethyl acetate, as a dye mordant, and analytical reagent. It is used in commercial nuclear power plants as a plating inhibitor on primary water piping.

Basic properties and structures
In anhydrous zinc acetate the zinc is coordinated to four oxygen atoms to give a tetrahedral environment, these tetrahedral polyhedra are then interconnected by acetate ligands to give a range of polymeric structures. In contrast, most metal diacetates feature metals in octahedral coordination with bidentate acetate groups.
In zinc acetate dihydrate the zinc is octahedral, wherein both acetate groups are bidentate.

Basic zinc acetate
Heating Zn(CH3CO2)2 in a vacuum results in a loss of acetic anhydride, leaving a residue of basic zinc acetate, with the formula Zn4O(CH3CO2)6. This cluster compound has the tetrahedral structure shown below. This species closely resembles the corresponding beryllium compound, although it is slightly expanded with Zn-O distances ~1.97 vs ~1.63 Å for Be4O(OAc)6.

Application
Employed in the synthesis of layered Zn-arylphosphonates with potential application in sorption, ion exchange or catalysis.[2] Also used in the ultrasonic preparationof zinc sulfide nanoparticles coated on silica particles.
Used as a dietary supplement and in lozenges used to treat the common cold.
Preparation Note
Preparation of ZnSe nanostructures upon thermolysis of zinc acetate and selenourea in a mixture of octadecylamine and trioctylphosphine oxide.

Obtained in both anhydrous form and as a dihydrate. Both are white crystalline solids. The primary hazard is the threat posed to the environment. Immediate steps should be taken to limit spread to the environment. Used to preserve wood, to make other Zinc acetate compounds, as a food and feed additive.
Zinc acetate can be used for the treatment and prevention of Zinc acetate deficiency/its consequences, including stunted growth and acute diarrhea in children, and slowed wound healing. It is also utilized for boosting the immune system, treating the common cold and recurrent ear infections, as well as preventing lower respiratory tract infections [L2172].

Zinc acetate USP is used as/ an astringent in low concentrations and an irritant at high concentrations. It also has mild antibacterial actions similar to those of zinc sulfate. When applied to cuts, it exerts styptic action.
Orally administered zinc acetate inhibits copper absorption through the intestine. Oral zinc /acetate/ therapy /for Wilson's disease/ is probably a safe and effective maintenance treatment for patients who were initially treated with chelating agents, and seems to be an appropriate first-line therapy for presymptomatic and pregnant patients. Combination drug therapy of a chelating agent and zinc acetate has no advantages when compared with zinc only, during maintenance therapy.

Zinc acetate has been developed for the treatment of Wilson's disease, an inherited disease of copper accumulation and copper toxicity in brain and liver. Zinc acetate has been approved by the US FDA for maintenance therapy of adult and pediatric Wilson's disease patients but also has efficacy in the treatment of pregnant patients and presymptomatic patients from the beginning. It also has value as adjunctive therapy for the initial treatment of symptomatic patients. Zinc's mechanism of action involves induction of intestinal cell metallothionein (Mt), which blocks copper absorption from the intestinal track. A negative copper balance is caused by blockade not only of absorption of food copper but the blockade of reabsorption of the considerable amount of endogenously secreted copper in saliva, gastric juice and intestinal secretions. Zinc acetate is completely effective in controlling copper levels and toxicity in Wilson's disease, as are other anticopper agents. Zinc's major advantage over other anticopper agents is its extremely low level of toxicity. The only side effect is some degree of initial gastric irritation in approximately10% of patients, which usually decreases and becomes insignificant over time. As with all long-term therapies, compliance is a problem in some patients and dictates regular monitoring with 24 hr urine copper and zinc measurements. As with all anticopper therapies, over a long period of time, overtreatment and induction of copper deficiency can occur. This is to be avoided particularly in children because copper is required for growth.

Zinc acetate supplementation decreases the morbidity of lower respiratory tract infection in pediatric patients in the developing world. We sought to determine if zinc acetate mediates a specific inhibitory effect against the major cause of pediatric lower respiratory tract disease, respiratory syncytial virus (RSV). We determined the in vitro inhibitory effect of three zinc salts (zinc acetate, lactate, and sulfate) on the replication of RSV at various concentrations of 10 and 1 mM and 100 and 10 microM. The degree of inhibition of RSV replication was examined in the presence of zinc acetate during preincubation, adsorption, or penetration and was compared with that caused by salts of other divalent cations. Complete inhibition of RSV plaque formation was observed at 1 and 10 mM, representing reductions that were > or =10(6)-fold. At the lowest concentration tested, 10 uM, we observed >or=1000-fold reductions in RSV yield when zinc acetate was present during preincubation, adsorption, penetration, or egress of virus. The therapeutic indices, determined as ratios of 50% toxicity concentration to 50% inhibitory concentration, were 100, 150, and 120 for zinc acetate, zinc lactate, and zinc sulfate, respectively. The inhibitory effect of zinc salts on RSV was concentration dependent and was not observed with other salts containing divalent cations such as calcium, magnesium, and manganese. RSV plaque formation was prevented by pretreatment of HEp-2 cell monolayer cultures with zinc acetate or by addition of zinc to methylcellulose overlay media after infection. The results of this study suggest that zinc mediates antiviral activity on RSV by altering the ability of the cell to support RSV replication.

Zinc acetate was used for the treatment and prophylaxis of hepatic copper toxicosis in 3 Bedlington Terriers and 3 West Highland White Terriers. Two dogs of each breed were treated for 2 years, and 1 of each breed for 1 year. A dosage of 200 mg of elemental zinc acetate per day was required to achieve therapeutic objectives related to copper, which included a doubling of plasma zinc concentration to 200 ug/dl and a suppression of oral 64 copper absorption. The dosage was later reduced to 50 to 100 mg/day to avoid an excessive increase in plasma zinc concentration. The preliminary clinical results were good. Three dogs had mild to moderate active liver disease and high liver copper concentrations at the time of initiation of zinc acetate administration. Biopsy of the liver 2 years later revealed a reduction in hepatitis and copper concentrations. One other dog without active hepatitis also had a reduction in hepatic copper concentrations over a 2-year period. All 6 dogs have done well clinically. On the basis of these findings, we believe zinc acetate to be an effective and nontoxic treatment for copper toxicosis in dogs.

Zinc acetate is not recommended for the initial therapy of symptomatic patients because of the delay required for zinc-induced increase in enterocytic metallothionein and blockade of copper uptake. Symptomatic patients should be treated initially, using chelating agents. During initial therapy, neurological deterioration may occur as stores of copper are mobilized. Once initial therapy has been completed, and the patient is clinically stable, maintenance treatment with zinc acetate can be considered, but patients may be continued on initial therapy as clinically indicated.

Zinc acetate does appear in breast milk and zinc-induced copper deficiency in the nursing baby may occur. Therefore, it is recommended that women on zinc therapy not nurse their babies.
Transient elevations in serum amylase, lipase, and alkaline phosphatase have been observed in patients with Wilson's disease receiving zinc acetate therapy (25 or 50 mg elemental zinc 3 times daily) ... Whether the increase in these enzyme levels in serum is indicative of pancreatic injury remains questionable.
If this drug is used during pregnancy, the possibility of fetal harm appears remote. Because studies cannot rule out the possibility of harm, however, zinc acetate should be used during pregnancy only if clearly needed. While zinc acetate should be used during pregnancy only if clearly needed, copper toxicosis can develop during pregnancy if anti-copper therapy is stopped.

Absorption of zinc acetate
Zinc acetate is absorbed in the small intestine by a carrier-mediated mechanism [L2092]. Under regular physiologic conditions, transport processes of uptake do not saturate. The exact amount of zinc absorbed is difficult to determine because zinc acetate is secreted into the gut. Zinc administered in aqueous solutions to fasting subjects is absorbed quite efficiently (at a rate of 60-70%), however, absorption from solid diets is less efficient and varies greatly, dependent on zinc content and diet composition [L2092]. Generally, 33% is considered to be the average zinc acetate absorption in humans [L2092]. More recent studies have determined different absorption rates for various populations based on their type of diet and phytate to zinc molar ratio. Zinc acetate absorption is concentration dependent and increases linearly with dietary zinc up to a maximum rate [L20902]. Additionally zinc status may influence zinc acetate absorption. Zinc-deprived humans absorb this element with increased efficiency, whereas humans on a high-zinc diet show a reduced efficiency of absorption [L2092].

Route of Elimination
The excretion of zinc acetate through gastrointestinal tract accounts for approximately one-half of all zinc eliminated from the body [L2092]. Considerable amounts of zinc acetate are secreted through both biliary and intestinal secretions, however most is reabsorbed. This is an important process in the regulation of zinc balance. Other routes of zinc acetate excretion include both urine and surface losses (sloughed skin, hair, sweat) [L2092]. Zinc acetate has been shown to induce intestinal metallothionein, which combines zinc acetate and copper in the intestine and prevents their serosal surface transfer. Intestinal cells are sloughed with approximately a 6-day turnover, and the metallothionein-bound copper and zinc are lost in the stool and are thus not absorbed [L2103]. Measurements in humans of endogenous intestinal zinc acetate have primarily been made as fecal excretion; this suggests that the amounts excreted are responsive to zinc intake, absorbed zinc acetate and physiologic need [L2092]. In one study, elimination kinetics in rats showed that a small amount of ZnO nanoparticles was excreted via the urine, however, most of the nanoparticles were excreted via the feces [L2100].

The absorption of zinc from soluble zinc acetate, zinc sulfate ... and insoluble zinc oxide was compared in ten human volunteers who were dosed orally with 50 mg Zn in various forms separated by two weeks intervals. Bioavailability of zinc acetate from the various forms was compared on the basis of plasma zinc levels and area under the plasma curve (AUC) analysis. Plasma peak levels were observed after about 2.5 hours for all forms, but maximal plasma Zn concentration amounted to 221 and 225 ug/dL for the acetate and the sulphate form while the peak plasma level for Zn from the oxide was only 159 ug/dL. When AUC values for the different zinc acetate forms were compared, it appeared that the bioavailability of zinc oxide was about 60% of the bioavailability of the soluble forms.

Zinc acetate is released from food as free ions during its digestion. These freed ions may then combine with endogenously secreted ligands before their transport into the enterocytes in the duodenum and jejunum. [L2092]. Selected transport proteins may facilitate the passage of zinc acetate across the cell membrane into the hepatic circulation. With high intake, zinc acetate may also be absorbed through a passive paracellular route [L2092]. The portal system carries absorbed zinc acetate directly into the hepatic circulation, and then it is released into systemic circulation for delivery to various tissues. Although, serum zinc acetate represents only 0.1% of the whole body zinc, the circulating zinc turns over rapidly to meet tissue needs [L2092].

Zinc acetate has three primary biological roles: _catalytic_, _structural_, and _regulatory_. The catalytic and structural role of zinc is well established, and there are various noteworthy reviews on these functions. For example, zinc acetate is a structural constituent in numerous proteins, inclusive of growth factors, cytokines, receptors, enzymes, and transcription factors for different cellular signaling pathways. It is implicated in numerous cellular processes as a cofactor for approximately 3000 human proteins including enzymes, nuclear factors, and hormones [L2096]. Zinc promotes resistance to epithelial apoptosis through cell protection (cytoprotection) against reactive oxygen species and bacterial toxins, likely through the antioxidant activity of the cysteine-rich metallothioneins [A32419]. In HL-60 cells (promyelocytic leukemia cell line), zinc enhances the up-regulation of A20 mRNA, which, via TRAF pathway, decreases NF-kappaB activation, leading to decreased gene expression and generation of tumor necrosis factor-alpha (TNF-alpha), IL-1beta, and IL-8 [A32418]. There are several mechanisms of action of zinc acetate on acute diarrhea. Various mechanisms are specific to the gastrointestinal system: zinc acetate restores mucosal barrier integrity and enterocyte brush-border enzyme activity, it promotes the production of antibodies and circulating lymphocytes against intestinal pathogens, and has a direct effect on ion channels, acting as a potassium channel blocker of adenosine 3-5-cyclic monophosphate-mediated chlorine secretion. Cochrane researchers examined the evidence available up to 30 September 2016 [L2106]. Zinc acetate deficiency in humans decreases the activity of serum _thymulin_ (a hormone of the thymus), which is necessary for the maturation of T-helper cells.  Because IL-2 production (Th(1) cytokine) is decreased, this causes decreased activity of natural-killer-cell (NK cell) and T cytolytic cells, normally involved in killing viruses, bacteria, and malignant cells [A3424]. In humans, zinc acetate deficiency may lead to the generation of new CD4+ T cells, produced in the thymus. In cell culture studies (HUT-78, a Th(0) human malignant lymphoblastoid cell line), as a result of zinc deficiency, nuclear factor-kappaB (NF-kappaB) activation, phosphorylation of IkappaB, and binding of NF-kappaB to DNA are decreased and this results in decreased Th(1) cytokine production [A32417]. In another study, zinc supplementation in human subjects suppressed the gene expression and production of pro-inflammatory cytokines and decreased oxidative stress markers [A3424]. In HL-60 cells (a human pro-myelocytic leukemia cell line), zinc acetate deficiency increased the levels of TNF-alpha, IL-1beta, and IL-8 cytokines and mRNA. In such cells, zinc acetate was found to induce A20, a zinc finger protein that inhibited NF-kappaB activation by the tumor necrosis factor receptor-associated factor pathway. This process decreased gene expression of pro-inflammatory cytokines and oxidative stress markers [A32417]. The exact mechanism of zinc in acne treatment is poorly understood. However, zinc is considered to act directly on microbial inflammatory equilibrium and facilitate antibiotic absorption when used in combination with other agents. Topical zinc acetate alone as well as in combination with other agents may be efficacious because of its anti-inflammatory activity and ability to reduce P. acnes bacteria by the inhibition of P. acnes lipases and free fatty acid levels [L2102].

The active moiety in zinc acetate is zinc acetate cation. Regardless of the ligand, zinc blocks the intestinal absorption of copper from the diet and the reabsorption of endogenously secreted copper such as that from the saliva, gastric juice and bile. Zinc acetate induces the production of metallothionein in the enterocyte, a protein that binds copper thereby preventing its serosal transfer into the blood. The bound copper is then lost in the stool following desquamation of the intestinal cells.
The mechanism of zinc's anticopper action is unique. It induces intestinal cell metallothionein, which binds copper and prevents its transfer into blood. As intestinal cells die and slough, the contained copper is eliminated in the stool. Thus, zinc acetate prevents the intestinal absorption of copper.

In the case where zinc acetate removal is the only consideration and recovery is not warranted, removal by precipitation can be accomplished by standard pH adjustment through lime addition, precipitation and flocculation, and sedimentation, employing standard waste treatment equipment, operating data for existing chemical precipitation units indicate that levels of 1 mg/l or less of zinc acetate are readily obtainable with lime precipitation, although assurance of consistent removal of precipitated zinc to lower levels from the effluent stream may require filtration. 
Organic zinc salts such as zinc aspartate, zinc orotate, zinc histidine and zinc acetate protected mice against the lethality of an acute intraperitoneal challenge with ethanol. A similar activity was also provided by salts of cobalt, zirconium, lithium, and magnesium. Organic zinc salts acted synergistically with sulfhydryl compounds in protecting the mice and potentiation between the two categories of agents was seen.

The effect of zinc acetate on mercuric chloride induced lipid peroxidation in the rat kidney was investigated. The rats received zinc acetate (2.0 nmol/kg, po) for 2 days before being given mercuric chloride (15 umol/kg, sc) and were killed 6, 12, and 24 hr after the last injection. Lipid peroxidation occurred in the rat kidney 12 hr after mercury administration, and this mercury induced lipid peroxidation was significantly reduced by zinc pretreatment. A decrease in vitamin C and E contents in the kidney was observed 12 hr after the administration of mercury, and this decrease was prevented by zinc pretreatment. In the kidney of rats pretreated with zinc, the activities of the protective enzymes, glutathione peroxidase and glucose-6-phosphate dehydrogenase, were increased after mercury injection. Non-protein sulfhydryl content (mostly glutathione) also rose markedly.

In comparison with similar experiments in which no zinc acetate was used, the addition of small amounts of zinc acetate to sodium N-methyl-N-dithiocarboxyglucamine produces a significant increase in the amount of cadmium mobilized from the liver and kidneys of mice loaded ip with 10 mg cadmium chloride/kg 2 wk prior to the initiation of treatment. Neither treatment results in the transport of significant amounts of cadmium to the brain. The injection of zinc acetate alone did not produce this effect. Experiments in which zinc acetate in drinking water was administered to cadmium loaded animals showed that the liver and kidney cadmium levels were significantly increased, presumably via zinc mediated processes.

Wistar rats were injected (ip) either with 5 mg cis-diamminedichloro-platinum-II (cis-DDP)/kg, or pretreated with zinc acetate and then injected with cis-DDP. The zinc acetate pretreatment significantly increased the binding of zinc (Zn) and copper (Cu) to both the renal and hepatic metallothioneins, but the proportion of cytosolic platinum associated with metallothioneins in the kidney tissue slightly reduced, and that in the liver showed no difference in comparison to rats treated with cis-diamminedichloro-platinum-II only. The results indicate that an increased cis-diamminedichloro-platinum-II biosynthesis the zinc pretreatment may not correspondingly increase the binding of intracellular Pt to cis-diamminedichloro-platinum-II. In the zinc acetate pretreated rats, the renal tissue and subellular Pt levels were significantly lower (p less than 0.01) than those in untreated rats, although the liver levels showed practically no difference.
Treatment for acute zinc toxicity is supportive. After oral ingestion of zinc acetate or zinc salts, treatment should be directed toward control of nausea, vomiting, and diarrhea. Induced emesis, gastric lavage, or activated charcoal usually are unnecessary but may be useful in cases of substantial ingestion of zinc acetate tablets of capsules. ...Treatment of zinc-induced copper deficiency requires discontinuation of supplemental zinc and therapy with oral or iv copper if necessary. 

The effect of increasing the time interval between acute zinc acetate exposure and chelation therapy was studied in male Swiss mice. Cyclohexanediaminetetraacetic acid (CDTA), and diethylenetriaminepentaacetic acid (DTPA) were administered ip at 0, 0.25, 0.5, 2, 12, or 24 hr after ip administration of 0.40 mmol/kg of zinc acetate dihydrate. Chelating agents were given at doses equal to 1/3 of their respective LD50 values. Effectiveness of chelation therapy was determined by measuring the ability of the chelators to increase the elimination of zinc acetate and decrease the concentration of the metal in various tissues. Treatment with DTPA or CDTA increased significantly the urinary and fecal excretion of zinc when the chelators were administered at various times following zinc exposure. The greatest antidotal efficacy of the chelating agents was observed at 0.50 hr after zinc injection. Nevertheless, the effectiveness of DTPA and CDTA was decreasing when the chelators were administered later. DTPA was more effective than CDTA in the prevention of acute zinc acetate intoxication. CDTA would be considered as a possible alternative.

Researchers/ exposed groups of eight healthy women to 0, 15, 50, or 100 mg supplemental zinc as zinc acetate daily for 60 days (approximately 0, 0.25, 0.83, or 1.7 mg supplemental Zn/kg-day, assuming a reference female body weight of 60 kg) and evaluated effects on serum zinc and cholesterol levels. Zinc exposure resulted in significant, dose-related increases in serum zinc. In the highest exposure group only, plasma HDL-cholesterol was significantly reduced at 4 weeks of exposure, but not at any other timepoint examined. A direct correlation between dietary zinc and whole-blood copper was observed in treated subjects. The study authors noted that in the 50 and 100 mg groups, some bloating, nausea, and abdominal cramps were noted unless the supplement was taken with a large glass of water at mealtime.

Acute Exposure/ The dermal irritancy of six zinc compounds was examined in three animal models, In open patch tests involving five daily applications, zinc chloride (1% aqueous solution) was severely irritant in rabbit, guinea-pig and mouse tests, inducing epidermal hyperplasia and ulceration; aqueous zinc acetate (20%) was slightly less irritant ... Epidermal irritancy in these studies is related to the interaction of zinc ion with epidermal keratin. The compounds studied were not consistently bacteriostatic in the three species tested.

Acute Exposure/ Rats were treated with zinc acetate for four days. The zinc doses were 5 mg Zn/kg and 10 mg Zn/kg body weight respectively. Two groups of the zinc acetate-treated rats were later challenged with a single dose of CCl4 (1.5 mL/kg body weight). Compared to control animals, the plasma of rats treated with CCl4 showed hyperbilirubinemia, hypoglycemia, hypercreatinemia and hypoproteinemia. When the animals were however supplemented with zinc in form of zinc acetate before being dosed with CCl4, the 5 mg Zn/kg body weight of zinc acetate reversed the hypoproteinemia induced by CCl4, whereas the 10 mg Zn/kg body weight of zinc acetate reversed the hypoglycemia, hyperbilirubinemia and hypercreatinemia induced by CCl4. The 10 mg Zn/kg body weight of zinc acetate is more consistent in protecting against CCl4 hepatotoxicity. The possible mechanisms of protection are highlighted.

What is zinc acetate?
Zinc is a naturally occurring mineral. Zinc is important for growth and for the development and health of body tissues.
Zinc acetate is used to treat and to prevent zinc deficiency.
Zinc acetate may also be used for other purposes not listed in this medication guide.

Important Information
Before using zinc acetate, talk to your doctor, pharmacist, herbalist, or other healthcare provider. You may not be able to use zinc acetate if you have certain medical conditions.
Avoid taking this medication with foods that are high in calcium or phosphorus, which can make it harder for your body to absorb zinc acetate. Foods high in calcium or phosphorus include milk, cheese, yogurt, ice cream, dried beans or peas, lentils, nuts, peanut butter, beer, cola soft drinks, and hot cocoa.
Zinc acetate can make certain antibiotics less effective. Tell your doctor about all other medications you are using before you start taking zinc acetate.

Before taking this medicine
Before using zinc acetate, talk to your doctor, pharmacist, herbalist, or other healthcare provider. You may not be able to use zinc acetate if you have certain medical conditions.
It is not known whether zinc acetate will harm an unborn baby. Do not take zinc acetate without telling your doctor if you are pregnant or could become pregnant during treatment.
It is not known whether zinc acetate passes into breast milk or if it could harm a nursing baby. Do not use this medication without telling your doctor if you are breast-feeding a baby.
How should I take zinc acetate?
Use exactly as directed on the label, or as prescribed by your doctor. Do not use in larger or smaller amounts or for longer than recommended.
Take zinc acetate with a full glass of water.
Take zinc acetate with food if it upsets your stomach.
Your healthcare provider may occasionally change your dose to make sure you get the best results from zinc acetate. The recommended dietary allowance of zinc acetate increases with age. Follow your healthcare provider's instructions. You may also consult the National Academy of Sciences "Dietary Reference Intake" or the U.S. Department of Agriculture's "Dietary Reference Intake" (formerly "Recommended Daily Allowances" or RDA) listings for more information.
Store at room temperature away from moisture and heat.

What should I avoid while taking zinc acetate?
Avoid taking this medication with foods that are high in calcium or phosphorus, which can make it harder for your body to absorb zinc acetate. Foods high in calcium or phosphorus include milk, cheese, yogurt, ice cream, dried beans or peas, lentils, nuts, peanut butter, beer, cola soft drinks, and hot cocoa.

Zinc acetate side effects
Get emergency medical help if you have any of these signs of an allergic reaction: hives; difficulty breathing; swelling of your face, lips, tongue, or throat.

Synonyms:
Acetic acid, Zinc salt; Acetic acid, Zinc(II) salt; Dicarbomethoxyzinc; Zinc diacetate; Zinc acetate dihydrate; ZINC ACETATE; Zinc diacetate; 557-34-6; Zinc(II) acetate; Acetic acid, zinc salt; Dicarbomethoxyzinc; Zinc acetate anhydrous; Acetic acid, zinc(II) salt; Zinc di(acetate); Siltex CL 4; Zn(OAc)2; UNII-H2ZEY72PME; CCRIS 3471; Acetic acid, zinc salt (2:1); HSDB 1043; EINECS 209-170-2; NSC 75801; H2ZEY72PME; AI3-04465; CHEBI:62984; zincacetate; Zinc acetate, 99%, pure; NSC-75801; zinc (II) acetate; Zinc acetate,anhydrous; Zinc acetate [USAN]; zinc acetate carrageenan; ACMC-20aj8v; Zn(II)Ac2; ZA/CG; SCHEMBL51; Zinc Acetate (anhydrous); ZINC ACETATE BASIC; C4H6O4Zn; Zinc Acetate 35% 40M; (CH3CO2)2Zn; DSSTox_CID_18770; Zinc Acetate, Trace metals grade; Zinc acetate dihydrate; 5970-45-6; Zinc diacetate dihydrate; Zinc(II) acetate dihydrate; Acetic acid zinc salt; UNII-FM5526K07A; Zinc acetate [USP]; ZINC OXIDE; 1314-13-2; Zinc White; oxozinc; Amalox; Chinese White; Snow white; Emanay zinc oxide; Felling zinc oxide; Zinc oxide (ZnO); Akro-zinc bar 85; Zinc monoxide; Flowers of zinc; Azo-33; Outmine; Supertah; Zincite; Zincoid; Azodox; Ozide; Ozlo; Zincum Oxydatum; Zinci Oxicum; Zinci Oxydum; Flores de zinci; Hubbuck's White; Blanc de Zinc; Unichem ZO; Vandem VAC; Vandem VOC; çinko oksit; Vandem VPC; Green seal-8; Philosopher's wool; White seal-7; K-Zinc; Powder base 900; Protox type 166; Protox type 167; Protox type 168; Protox type 169; Protox type 267; Protox type 268; Akro-zinc bar 90; Azodox-55; Azodox-55TT; Red Seal 9; EMAR; CI Pigment white 4; Electrox 2500; Actox 14; Actox 16; Kadox 15; Kadox 72; Kadox-25; Zinc oxide [USAN]; Zinca 20; Protox 166; Protox 168; Protox 169; Caswell No. 920; Electox 2500; Cadox XX 78; Actox 216; Acetic acid, zinc salt, dihydrate; Zinc acetate, dihydrate; MFCD00066961; FM5526K07A; Zinc acetate (USP); Octan zinecnaty; Zinc acetate dihydrate, 98%, extra pure; Zinc acetate dihydrate, 98+%, ACS reagent; Zinc acetate dihydrate, 97%, specified according to the requirements of USP; Galzin (TN); Zinc acetate, dihydrate; Zinc; Zn; Zinc dust; cinc; Zinc, elemental; Zinc(1+); zincide; Merrillite; Rheinzink; Jasad; Blue powder; Granular zinc; Zinc powder; Emanay zinc dust; Zincum metallicum; Asarco L 15; Zinc (fume or dust); zincum; Zinc, ion (Zn1+); Zink; Lead refinery vacuum zinc; Zinc(1-); UNII-J41CSQ7QDS; Zinc (metallic); Acetic acid, Zinc salt; Acetic acid, Zinc(II) salt; Dicarbomethoxyzinc; Zinc diacetate; Zinc acetate dihydrate; ZINC ACETATE; Zinc diacetate; 557-34-6; Zinc(II) acetate; Acetic acid, zinc salt; Dicarbomethoxyzinc; Zinc acetate anhydrous; Acetic acid, zinc(II) salt; Zinc di(acetate); Siltex CL 4; Zn(OAc)2