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General Description:

Zinc acetate is a chemical compound identified by the CAS number 557-34-6. It is known for its distinct pharmacological properties and applications.

Indications:

This drug is primarily indicated for: Zinc can be used for the treatment and prevention of zinc 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 . Its use in specific medical scenarios underscores its importance in the therapeutic landscape.

Metabolism:

Zinc acetate undergoes metabolic processing primarily in: Zinc 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. . Selected transport proteins may facilitate the passage of zinc across the cell membrane into the hepatic circulation. With high intake, zinc may also be absorbed through a passive paracellular route . The portal system carries absorbed zinc directly into the hepatic circulation, and then it is released into systemic circulation for delivery to various tissues. Although, serum zinc represents only 0.1% of the whole body zinc, the circulating zinc turns over rapidly to meet tissue needs . This metabolic pathway ensures efficient processing of the drug, helping to minimize potential toxicity and side effects.

Absorption:

The absorption characteristics of Zinc acetate are crucial for its therapeutic efficacy: Zinc is absorbed in the small intestine by a carrier-mediated mechanism . Under regular physiologic conditions, transport processes of uptake do not saturate. The exact amount of zinc absorbed is difficult to determine because zinc 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 . Generally, 33% is considered to be the average zinc absorption in humans . More recent studies have determined different absorption rates for various populations based on their type of diet and phytate to zinc molar ratio. Zinc absorption is concentration-dependent and increases linearly with dietary zinc up to a maximum rate . Additionally zinc status may influence zinc absorption. Zinc-deprived humans absorb this element with increased efficiency, whereas humans on a high-zinc diet show a reduced efficiency of absorption . The drug's ability to rapidly penetrate into cells ensures quick onset of action.

Half-life:

The half-life of Zinc acetate is an important consideration for its dosing schedule: The half-life of zinc in humans is approximately 280 days . This determines the duration of action and helps in formulating effective dosing regimens.

Protein Binding:

Zinc acetate exhibits a strong affinity for binding with plasma proteins: Approximately 60-70% of the zinc in circulation is bound to albumin. Any condition that alters serum albumin concentration may have a secondary effect on serum zinc levels . This property plays a key role in the drug's pharmacokinetics and distribution within the body.

Route of Elimination:

The elimination of Zinc acetate from the body primarily occurs through: The excretion of zinc through gastrointestinal tract accounts for approximately one-half of all zinc eliminated from the body . Considerable amounts of zinc 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 excretion include both urine and surface losses (sloughed skin, hair, sweat) . Zinc has been shown to induce intestinal metallothionein, which combines zinc 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 . Measurements in humans of endogenous intestinal zinc have primarily been made as fecal excretion; this suggests that the amounts excreted are responsive to zinc intake, absorbed zinc and physiologic need . 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 . Understanding this pathway is essential for assessing potential drug accumulation and toxicity risks.

Volume of Distribution:

Zinc acetate is distributed throughout the body with a volume of distribution of: A pharmacokinetic study was done in rats to determine the distribution and other metabolic indexes of zinc in two particle sizes. It was found that zinc particles were mainly distributed to organs including the liver, lung, and kidney within 72 hours without any significant difference being found according to particle size or rat gender . This metric indicates how extensively the drug permeates into body tissues.

Clearance:

The clearance rate of Zinc acetate is a critical factor in determining its safe and effective dosage: In one study of healthy patients, the clearance of zinc was found to be 0.63 ± 0.39 μg/min . It reflects the efficiency with which the drug is removed from the systemic circulation.

Pharmacodynamics:

Zinc acetate exerts its therapeutic effects through: Zinc is involved in various aspects of cellular metabolism. It has been estimated that approximately 10% of human proteins may bind zinc, in addition to hundreds of proteins that transport and traffic zinc. It is required for the catalytic activity of more than 200 enzymes, and it plays a role in immune function wound healing, protein synthesis, DNA synthesis, and cell division. Zinc is an essential element for a proper sense of taste and smell and supports normal growth and development during pregnancy, childhood, and adolescence. It is thought to have antioxidant properties, which may be protective against accelerated aging and helps to speed up the healing process after an injury; however, studies differ as to its effectiveness. Zinc ions are effective antimicrobial agents even if administered in low concentrations . Studies on oral zinc for specific conditions shows the following evidence in various conditions : Colds: Evidence suggests that if zinc lozenges or syrup are taken within 24 hours after cold symptoms start, the supplement may shorten the length of colds. The use intranasal zinc has been associated with the loss of the sense of smell, in some cases long-term or permanently . Wound healing: Patients with skin ulcers and decreased levels of zinc may benefit from oral zinc supplements . Diahrrea: Oral zinc supplements can reduce the symptoms of diarrhea in children with low levels of zinc, especially in cases of malnutrition . The drug's ability to modulate various physiological processes underscores its efficacy in treating specific conditions.

Mechanism of Action:

Zinc acetate functions by: Zinc 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 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 . 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 . 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 . There are several mechanisms of action of zinc on acute diarrhea. Various mechanisms are specific to the gastrointestinal system: zinc 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 . Zinc deficiency in humans decreases the activity of serum _thymulin_ (a hormone of the thymus), which is necessary for the maturation of T-helper cells. T-helper 1 (Th(1)) cytokines are decreased but T-helper 2 (Th(2)) cytokines are not affected by zinc deficiency in humans . The change of _Th(1)_ to _Th(2)_ function leads to cell-mediated immune dysfunction. 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 . In humans, zinc 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 . In another study, zinc supplementation in human subjects suppressed the gene expression and production of pro-inflammatory cytokines and decreased oxidative stress markers . In HL-60 cells (a human pro-myelocytic leukemia cell line), zinc deficiency increased the levels of TNF-alpha, IL-1beta, and IL-8 cytokines and mRNA. In such cells, zinc 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 . 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 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 . This mechanism highlights the drug's role in inhibiting or promoting specific biological pathways, contributing to its therapeutic effects.

Toxicity:

Categories:

Zinc acetate is categorized under the following therapeutic classes: Acetates, Acids, Acyclic, Agents for Treatment of Hemorrhoids and Anal Fissures for Topical Use, Alimentary Tract and Metabolism, Metal cations, Metal divalent cations, Minerals, Various Alimentary Tract and Metabolism Products, Vasoprotectives, Zinc Compounds. These classifications highlight the drug's diverse therapeutic applications and its importance in treating various conditions.