Zinc gluconate 50mg tablets

Abstract Background: Hemodialysis patients often suffer from several complications such as malnutrition and skin abnormalities. We hypothesized that zinc supplementation may improve these complications. The aim of the present study was to examine the effects of zinc gluconate supplementation on malnutrition and skin abnormalities. Methods: In this parallel randomized, double-blind, clinical trial, patients in the zinc group received 210 mg zinc gluconate (equivalent to 30 mg elemental zinc) per day. Skin abnormalities (i.e. xerosis and pruritus), body composition, anthropometric variables, handgrip strength, and appetite (including hunger, fullness, desire to eat, and prospective food consumption) were measured at the beginning and end of the study. Results: Eighty-seven hemodialysis patients were randomly assigned to the zinc ( n = 44) or placebo ( n = 43) group for 12 weeks, After this period, 75 patients ( N = 38 in the zinc group and 37 in the placebo group) remained in the study. In this study, no specific side effects of zinc supplementation were observed and twelve participants were lost to follow-up ( n = 6 in each group) because of migration, kidney transplantation, death, dialysis access infection, and personal reasons. Zinc supplementation had beneficial effects on hunger) 95% CI: 9/55 (3/67-15/42)), desire to eat) 95% CI: 7/03 (1/82-12/24)), and prospective food consumption) 95% CI: 3/46 (0/3-14/1)) compared with placebo. Also, zinc improved pruritus) 95% CI: −0/52 (−0/82 to − 0/22)). We observed no changes in body composition, anthropometric variables, handgrip strength, and xerosis in the zinc group compared with the placebo. Conclusions: This randomized clinical trial showed that zinc supplementation yielded beneficial effects on appetite and pruritus in hemodialysis patients.

Abstract licence: CC BY-NC-SA

Objective The aim of the study is to investigate the function and mechanism of Zinc Gluconate (ZG) on intestinal mucosal barrier damage in antibiotics and Lipopolysaccharide (LPS)-induced mice. Methods We established a composite mouse model by inducing intestinal mucosal barrier damage using antibiotics and LPS. The animals were divided into five groups: Control (normal and model) and experimental (low, medium, and high-dose ZG treatments). We evaluated the intestinal mucosal barrier using various methods, including monitoring body weight and fecal changes, assessing pathological damage and ultrastructure of the mouse ileum, analyzing expression levels of tight junction (TJ)-related proteins and genes, confirming the TLR4/NF-κB signaling pathway, and examining the structure of the intestinal flora. Results In mice, the dual induction of antibiotics and LPS led to weight loss, fecal abnormalities, disruption of ileocecal mucosal structure, increased intestinal barrier permeability, and disorganization of the microbiota structure. ZG restored body weight, alleviated diarrheal symptoms and pathological damage, and maintained the structural integrity of intestinal epithelial cells (IECs). Additionally, ZG reduced intestinal mucosal permeability by upregulating TJ-associated proteins (ZO-1, Occludin, Claudin-1, and JAM-A) and downregulating MLCK, thereby repairing intestinal mucosal barrier damage induced by dual induction of antibiotics and LPS. Moreover, ZG suppressed the TLR4/NF-κB signaling pathway, demonstrating anti-inflammatory properties and preserving barrier integrity. Furthermore, ZG restored gut microbiota diversity and richness, evidenced by increased Shannon and Observed features indices, and decreased Simpson’s index. ZG also modulated the relative abundance of beneficial human gut bacteria ( Bacteroidetes , Firmicutes , Verrucomicrobia , Parabacteroides , Lactobacillus , and Akkermansia ) and harmful bacteria ( Proteobacteria and Enterobacter ), repairing the damage induced by dual administration of antibiotics and LPS. Conclusion ZG attenuates the dual induction of antibiotics and LPS-induced intestinal barrier damage and also protects the intestinal barrier function in mice.

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Sodium gluconate improves aqueous zinc-ion battery performance by in situ insertion of Na + in the V 2 O 5 cathode for stability, while disrupting the solvated structure of Zn 2+ at the anode to inhibit dendrite formation and corrosion. Aqueous zinc-ion batteries (AZIBs) are gaining attention owing to their affordability, high safety, and high energy density, making them a promising solution for large-scale energy storage. However, their performance is hampered by the instability of both the anode-electrolyte interface and the cathode-electrolyte interface. The use of sodium gluconate (SG), an organic sodium salt with multiple hydroxyl groups, as an electrolyte additive is suggested. Experimental and theoretical analyses demonstrate that Na + from SG can intercalate and deintercalate within the associated V 2 O 5 cathode during in situ electrochemical processes. This action supports the layered structure of V 2 O 5 , prevents structural collapse and phase transitions, and enhances Zn 2+ diffusion kinetics. Additionally, the gluconate anion disrupts the original Zn 2+ solvation structure, mitigates water-induced side reactions, and suppresses Zn dendrite growth. The synchronous regulation of both the V 2 O 5 cathode and Zn anode by the SG additive leads to considerable performance improvements. Zn||Zn symmetric batteries demonstrate a cycle life exceeding 2800 h at 0.5 mA cm −2 and 1 mAh cm −2 . In Zn||V 2 O 5 full batteries, a high specific capacity of 288.92 mAh g −1 and capacity retention of 82.29% are maintained over 1000 cycles at a current density of 2 A g −1 . This multifunctional additive strategy offers a new pathway for the practical application of AZIBs.

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Abstract Hard carbon serves as a highly promising anode material for sodium‐ion batteries due to its stable structure and cost‐effectiveness. Although the hard template method is commonly employed to enhance the sodium storage capacity, the reported process steps are complicated. In this study, we introduced a facile approach by utilizing ZnO as a self‐sacrificed template to engineer pore structures with one step for template removal without using harmful chemicals. Our investigations reveal that pretreatment of the material before carbonization can reduce the specific surface area and defect degree of the final hard carbon. When utilized as an anode material, the as‐prepared hard carbon demonstrated a reversible capacity of 334 mAh g −1 at 0.05 A g −1 with an initial Coulombic efficiency of 84 %. Even at a high current density of 2 A g −1 , the capacity stabilized at 183 mAh g −1 after 1000 continuous cycles. Electrochemical storage behavior and ex‐situ Raman spectroscopy unveiled insights into the potential sodium storage mechanism. These findings present a new approach to enhancing the reversible properties of hard carbon anode materials for high‐performance sodium‐ion batteries.

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Atopic dermatitis (AD) is a chronic inflammatory skin condition with complex causes involving immune factors. The presence of essential trace elements that support immune system function can influence the development of this condition. This study investigated how serum trace elements impact the pathogenesis of atopic dermatitis. Upon analyzing serum microelements in AD patients and control subjects, it was observed that patients with AD had notably lower zinc levels. Genomic analysis of AD skin revealed distinct gene expression patterns, specifically the increased expression of CXCL10 in the epidermis. The heightened levels of CXCL10 in AD skin lesions were found to correlate with reduced serum zinc levels. Treatment with zinc gluconate showed reduced chemotactic response and CXCL10 release, suggesting its potential to regulate CXCL10 expression of keratinocytes in AD. The mechanism behind this involved the downregulation of STAT phosphorylation through activating PPARα. In the AD-like dermatitis mouse model, zinc gluconate therapy decreased serum IgE levels, alleviated skin lesion severity, reduced skin thickness, and lowered CXCL10 expression, demonstrating its efficacy in managing AD-like skin conditions. These findings indicate that zinc gluconate can reduce inflammation in keratinocytes by activating PPARα, inhibiting STAT signaling, and decreasing CXCL10 release, thus highlighting its potential as a therapeutic target for AD.

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BACKGROUND: Chemical castration of male animals is an alternative to surgical castration for inducing azoospermia, consequent sterility. Intra-testicular injection of zinc gluconate has been used for chemical castration in several animal species. However, its application to equine species, such as donkeys, has yet to be reported. This study aimed to evaluate the use of zinc gluconate for the chemical castration of male donkeys and to compare its effectiveness relative to routine surgical castration. For this purpose, investigations of serum testosterone and anti-Müllerian hormone levels, testicular ultrasonographic echogenicity, and histopathological findings were performed. METHODS: Fourteen clinically healthy adult male donkeys were randomly and equally divided into two groups. The donkeys in group I (n = 7) underwent surgical castration. The donkeys in group II (n = 7) received intra-testicular zinc gluconate injections. The donkeys were kept under close clinical observation for 60 days. Abnormalities in donkey behavior and gross alterations in the external genitalia were recorded daily. Serum testosterone and anti-Müllerian hormone (AMH) levels were measured 15 days before the start of the treatment and 15, 30, 45, and 60 days after treatment. The testicles of group II donkeys were evaluated ultrasonographically. At the end of the study, the testes were removed and histologically examined. RESULTS: Serum testosterone levels significantly declined compared to pre-castration levels in surgically castrated donkeys (group I), but donkeys exposed to chemical castration (group II) showed a non-significant reduction in testosterone levels. Donkeys in the surgical group had considerably lower serum AMH levels. In contrast, there was a non-significant (p > 0.05) increase in AMH levels in the chemical group compared with the pre-sterilization level. In addition, ultrasonographic examination revealed that the testicular echo-density had changed, as observed by a few scattered hyperechoic regions throughout the entire testis parenchyma. The histopathological investigation confirmed the presence of necrosis of the spermatogenic epithelium, increased thickness of the basement membrane of the seminiferous tubules, marked interstitial fibrosis, and shrinkage of the seminiferous tubules. Furthermore, syncytial giant cells were present in the lumen of seminiferous tubules and were associated with Sertoli cell vacuolation. Donkeys subjected to chemical castration (group II) had orchitis, as confirmed histopathologically. CONCLUSION: Intra-testicular injection of zinc gluconate resulted in histopathological and ultrasonographic testicular changes in adult male donkeys, which may affect their reproductive potential. However, it did not significantly alter serum testosterone or AMH levels, indicating that it cannot be used as a substitute for surgical castration in male donkeys.

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