Introduction
Zinc L-carnosine (ZnC), also known as ZnC, is a chelate compound containing L-carnosine and zinc. Zinc is an essential mineral found in meat, eggs, shellfish, cheese, beans and tofu. Zinc is an essential mineral and is part of many enzymes that are critical for cell proliferation during cell repair, particularly in epithelial and epidermal cells]. Therefore, it is required for wound healing in the skin, connective tissue, and intestinal lining (especially epithelial tissue). Zinc deficiency, whether due to dietary, genetic, or other causes, can lead to pathological conditions such as growth retardation, skin symptoms, and dysgeusia.
L-Carnosine is also a part of ZnC. β-Alanyl-l-histidine is a dipeptide and a chelator of metal ions. It is found in the muscles of vertebrate animals and therefore in edible meat. It has been shown to exert protective effects in wound healing, immune function, diabetes, and vision loss, which is thought to be due to its role as a buffer and antioxidant.
The combination or chelation of zinc and carnosine to create ZnC is said to have better health benefits than either alone, as carnosine enhances zinc absorption due to its solubility, perhaps because it releases it in a delayed/extended release manner. Zinc is transported into tissue. In the United States, ZnC is licensed as a dietary zinc supplement and possible adjunct to promote restoration of gastric lining health in patients with peptic ulcer disease. Known as PepZin GI™ - XSTO, this is the only form of ZnC reviewed for safety and human use by the U.S. Food and Drug Administration (FDA) and was granted "New Dietary Ingredient" status in 2002. While several studies report its efficacy in restoring the gastric mucosa, there is evidence that it can also restore tissue in other parts of the gastrointestinal tract. For example, there are studies supporting its role in the treatment of taste disorders, gastrointestinal disorders, skin, liver, and oral mucositis caused by chemotherapy and/or radiation therapy. This makes sense considering that these soft, moist tissues are lined with epithelial tissue, and zinc plays a key role in maintaining the health and repair of epithelial tissue.
Oral mucositis is a common complication of cytotoxic radiation therapy and/or chemotherapy, affecting 75% of high-risk patients. This happens to almost every head and neck cancer patient who receives radiation therapy. It is associated with severe pain, odynophagia, dysgeusia, malnutrition, and dehydration, seriously impairing patients' quality of life. Although this is a very serious and common side effect of radiation and/or chemotherapy, affecting length of hospital stay and overall outcome, treatment options are few and alternative treatments with established safety and effectiveness are needed. Therefore, the purpose of this review is to discuss research related to ZnC, a potential therapeutic approach, and explore its benefits, particularly in the treatment of diseases associated with damaged epithelial cells.
Mechanism of action of ZnC
Several studies have shown that ZnC can reduce gastric lesions associated with gastric ulcers and accelerate the healing process in animal models. Its main mechanism of action is thought to be related to its anti-inflammatory and antioxidant properties. For example, in an ethanol-induced rat gastric injury model, inflammatory cytokines (such as interleukin 1β, interleukin 8, interleukin 6, and tumor necrosis factor) were increased in a dose-dependent manner compared with the group receiving ZnC. way reduced. Control group. It has been reported that NF-kB (nuclear factor kappa light chain enhancer of activated B cells), one of the major transcription factors that regulates the expression of genes related to inflammation and immune response, is inhibited by ZnC supplementation. Several in vitro and animal models support these findings. Furthermore, in the rat model, antioxidant markers, such as superoxide dismutase-1, superoxide dismutase-2, heme oxygenase-1, Peroxiredoxin-1 and peroxiredoxin-V were increased. Other studies have supported these findings. In addition, growth factors such as vascular endothelial growth factor, nerve growth factor, and platelet-derived growth factor were significantly increased in the group that received ZnC. An additional mechanism of action by which ZnC exerts its beneficial effects is through heat shock proteins, which have been shown to have cytoprotective effects. ZnC supplementation has been reported to increase heat shock proteins in rodent models. The antioxidant function of ZnC is supported by in vitro studies as well as human intervention studies. For example, a 12-week placebo-controlled study of participants aged 65 to 85 years with low plasma zinc levels (less than 0.77 mg/l (11.77 mM) (n D 90)) was randomized to receive ZnC supplementation agent or placebo. - The supplemented group took daily ZnC tablets containing 86.9 mg ZnC (equivalent to 20 mg zinc). Plasma ferric reducing capacity and erythrocyte superoxide dismutase (eSOD) activity were found to be higher in the ZnC supplemented group compared with baseline; however, only eSOD activity was significantly higher than in the placebo group.
An in vitro study examined the effects of ZnC on the activity of cells involved in early and late stages of healing. The pro-migratory restorative activity of ZnC was evaluated in a damaged monolayer assay system with serial micrographs using the human colon cancer cell line HT-29. The effect on cell proliferation was assessed by [3H]thymidine incorporation assay using the human intestinal cell lines IEC-6 and HT-29 and the rat intestinal epithelial cell line RIE-1. Addition of ZnC in HT29 cells induced pro-migratory activity in a dose-dependent manner, with the maximum effect observed at 100 μM, resulting in a significant ( p < 0.01) approximately doubling of the wound closure rate. Addition of ZnC increased the proliferation of HT29 and RIE-1 cells in a typical bell-shaped dose-response manner. Peak stimulation (approximately 160% above baseline levels) occurred at 34 μM in HT29 and RIE-1 cells ( p < 0.01 compared to controls). No pro-stimulatory effect of ZnC was observed in IEC-6 cells. The authors concluded that ZnC, at concentrations similar to those likely present in the intestinal lumen, is capable of stimulating early and later stages of intestinal repair when tested using an in vitro intestinal injury model. Although this study was conducted in colon cells, it could be applied to other epithelial cells as well. go:
Oral mucositis
Oral mucositis is a common complication of cytotoxic radiation therapy and/or chemotherapy. This happens to almost every head and neck cancer patient who receives radiation therapy. It is associated with severe pain, odynophagia, dysgeusia, malnutrition, and dehydration, seriously impairing patients' quality of life. It may be the reason for prolonged hospitalization or even for premature cessation of treatment. Therefore, strategies to prevent mucositis may improve outcomes and reduce hospital stay. A prospective study was conducted to evaluate the feasibility and effectiveness of using ZnC in the form of an oral rinse to treat radiation-induced mucositis in patients with head and neck cancer undergoing radiation therapy. The ZnC concentration of the mouthwash was 37 mg/dl and was administered to the patient 4 times a day in the hospital and the mouthwash was kept in the mouth for 1 minute. This dose is equivalent to the recommended ZnC dose of 150 mg/day. Among patients who underwent irrigation, 29% developed grade 3 mucositis based on mucosal examination and 39.3% based on self-reported symptoms. Among those who did not receive irrigation, 40% developed grade 3 based on mucosal examination and 60.7% based on self-reported symptoms. Mouthwash was well tolerated and the authors concluded that it is a promising treatment for mucositis.
Recent reports indicate that oral administration of ZnC alginate suspension (P-AG) can effectively prevent oral mucositis associated with head and neck cancer radiotherapy, high-dose chemotherapy, and hematopoietic stem cell pre-radiotherapy. A follow-up review of medical records identified the exact benefits of supplementation and concluded that P-AG reduces irradiation time and discharge time after completion of radiotherapy by preventing oral mucositis in patients with head and neck cancer. Similarly, a study using an 18.75 mg ZnC lozenge formulation demonstrated a significant 13% reduction in the severity of oral mucositis and a 13% reduction in analgesic use in patients receiving high-dose hematopoietic stem cell transplant chemotherapy.
ZnC has been shown to prevent oral mucositis in patients with other types of malignancies receiving radiochemotherapy. One study administered a mouthwash containing ZnC (0.5 g suspended in 20 mL of 5% sodium alginate), P-AG to 36 patients with hematological malignancies who underwent high-dose chemotherapy and radiotherapy followed by hematopoietic stem cell transplantation (HSCT). Rinse your mouth for 2 minutes a day after each 4 transplants, and then swallow it for 1 month. The control group rinsed their mouths with chamomile ring for 1 month after transplantation. ZnC rinses reduced the incidence of moderate to severe oral mucositis compared with controls treated with chamomile ring rinse (20% vs. 82% grade ≥2, p < 0.01; 0% grade ≥3 vs. 45 % , p < 0.01). Pain associated with oral mucositis was also significantly reduced ( p = 0.004), resulting in reduced analgesic use (28% vs. 73%, p = 0.025). P-AG reduced the incidence of xerostomia and dysgeusia, but the effect was not significant. On the other hand, washout had no effect on the incidence of other adverse events, tumor response rates, or survival. The authors concluded that ZnC rinses were found to be highly effective in preventing oral mucositis not only caused by chemoradiotherapy for head and neck cancer, but also from high-dose chemotherapy and radiotherapy followed by HSCT.
Ishihama et al. It was reported that ZnC mouthwash could effectively improve oral mucosal damage in 423 patients who had symptoms of oral mucosal damage due to cancer treatment. The effect of ZnC irrigation was examined according to cancer treatment methods: the success rate of stomatitis prevention, symptom improvement rate, pain prevention success rate, and symptom improvement rate were 68.5%, 84.4%, 75.4%, and 76.7%, respectively. Chemotherapy (n = 280 ) ; radiotherapy and chemotherapy treatments were 32.7%, 64.5%, 45.5% and 73.5% ( n = 95) respectively; the mortality rates of radiotherapy alone were 29.6%, 60.0%, 40.7% and 68.6%.
In addition to being effective in preventing mucositis, ZnC has also been shown to prevent esophagitis that occurs as a complication of radiochemotherapy. Patients with non-small cell lung cancer who received weekly combination chemotherapy with carboplatin and paclitaxel and concurrent thoracic radiation therapy were evaluated. Patients who received ZnC treatment ( n = 19) were compared with those who did not receive treatment ( n = 19). Comparing patients who received 60 mL of sodium alginate solution and 150 mg of ZnC orally three times per day before meals to patients who did not receive ZnC but received 20 mL of sodium alginate solution orally three times per day before meals: as well as the use of hydrogen throughout the course of radiation therapy Aluminum magnesium oxide gel. Doses of 37.5 or 75 mg ZnC twice daily significantly inhibited the development of grade ≥2 radiation esophagitis (HR, 0.397; 95% CI, 0.160-0.990; p = 0.047 ) . The median onset time of the control group was 21.0 days, while the value of the experimental group did not reach significance. ZnC supplementation reduced the incidence of >grade 2 esophagitis at lower doses of radiation but not at higher doses, suggesting that ZnC delays the onset of ≥grade 2 esophagitis.
for taste disorders
Dysgeusia is often associated with oral mucositis and other side effects of chemotherapy and radiation therapy. Dysgeusias are common worldwide but are poorly studied, possibly because they are not considered serious or life-threatening. However, they affect up to 90% of patients undergoing radiation therapy for head and neck cancer, affecting quality of life and can indirectly affect the outcome of more severe disease by reducing nutritional intake. Taste buds contain enzymes that require zinc and play an important role in taste function. Several studies have shown that zinc supplementation can improve taste in people with taste disorders that are not related to cancer. A randomized, double-blind, placebo-controlled trial evaluated the effect of ZnC on dysgeusia. A total of 107 subjects with non-cancer-related taste disorders were assigned to receive placebo, 75 mg, 150 mg, or 300 mg oral ZnC for 12 weeks. Taste was assessed using filter paper disks (PFD) and subjective questionnaires, and serum zinc was measured before and after supplementation. Subjects receiving the 300 mg dose showed significant improvement compared to the placebo group. Subjective reported symptom improvements were seen in the groups receiving the 150 mg and 300 mg doses. Serum zinc increased in a dose-dependent manner, with the group receiving the highest dose of ZnC showing a statistically significant increase from baseline. No serious adverse events were reported.
Another study evaluated the effects of supplementation with 150 mg of ZnC in 40 patients complaining of dysgeusia. Patients were screened for serum zinc levels and divided into two groups. The zinc-deficient dysgeusia group refers to patients with serum zinc less than 63 µg/dl and no history of other diseases; those with values above this value are placed in the idiopathic group. Both groups received 150 mg of ZnC for an average of 17.7 weeks. Subjective symptoms were measured via a visual analogue scale (VAS). There were no statistically significant differences in subjective symptoms between groups at baseline. Interestingly, the supplement significantly improved symptoms in both groups. There was no correlation between VAS scores and serum zinc levels at the end of the study, suggesting that zinc deficiency or impairment may exist even if serum zinc levels are not below recommended levels.
In a single-center retrospective study, subjects exhibiting grade 2 dysgeusia due to chemotherapy received 150 mg of ZnC twice daily until symptoms resolved. The control group was given chamomile mouthwash. The median recovery time was significantly shorter in the group receiving ZnC compared with the control group (63 days vs. 112 days, hazard ratio (HR) 1.778; 95% CI = 1.275.2.280; p = 0.019 ) . Multivariable regression analysis showed that pancreatic cancer and fluoropyrimidine use increased the risk of grade 2 dysgeusia. This is likely because pancreatic secretions are involved in zinc absorption. Additionally, subjects with pancreatic cancer did not respond as well to oral supplements as those without pancreatic cancer.
Intestinal mucosal integrity
ZnC is perhaps best known for its approval in Japan to treat gastric ulcers. In a randomized, controlled, double-blind study, 258 subjects diagnosed with gastric ulcers were randomly assigned to receive 150 mg of ZnC daily, placebo, or 800 mg of cetroxal hydrochloride, a known mucosal protective agent. agent) or its placebo for 8 weeks. Endoscopy was performed before and after treatment and subjective measures of symptoms were collected. At 4 weeks, symptoms in the significantly improved category improved by 61% in the ZnC group and by 61.5% in the cetraxate group. At week 8, this increased to 75% in the ZnC group, a significant improvement compared to 72% in the cetraxate group. The endoscopic cure rates were 26.3% and 16.2% in the ZnC group and cetraxate group at 4 weeks, and 60.4% and 46.2% in the ZnC group and cetraxate group at 8 weeks. This suggests that ZnC may relieve symptoms and improve gastric ulcers better than known mucosal protectants. Another study conducted by the same group showed improvements in symptoms and endoscopic healing rates at all three doses of 50, 75, or 100 mg taken twice daily. Other human clinical trials support these results using doses of 50, 75, and 100 mg twice daily.
In a rat model of ethanol-induced gastric injury, ZnC treatment reduced the gastric ulcer index in rats and showed a significant ulcer healing effect similar to the gastric mucosal protective agent rebamipide. Similarly, in an animal model of aspirin-induced gastroduodenal injury, ZnC supplementation had a significant ulcer healing effect compared with the placebo treatment group. Furthermore, a study using an acetate-induced rat model reported that the ZnC-treated group showed significant antiulcer and healing effects compared with the control group. These results are most likely a result of the anti-inflammatory and antioxidant functions of ZnC. This function of ZnC helps explain the many other benefits it can exert throughout the gastrointestinal tract.
ZnC has been reported to stimulate multiple aspects of intestinal mucosal integrity. In vitro studies using pro-migration (damaged bilayer) and proliferation ([(3)H]-thymidine incorporation) assays in human colon (HT29), rat intestinal epithelial (RIE), and canine kidney epithelial cells demonstrated that ZnC stimulates cell migration and proliferation and reduces the amount of gastric and small intestinal damage in rats and mice. In vivo studies used a rat gastric injury model (indomethacin/restraint) and a mouse small intestinal injury model (indomethacin). Oral administration of ZnC reduced gastric damage (75% reduction at 5 mg/mL) and small intestinal damage (50% reduction in villus shortening at 40 mg/mL; both p < 0.01 ) . In a crossover study of 10 healthy human subjects, indomethacin (50 mg three times daily) was compared with ZnC (37.5 mg twice daily) or placebo in the intestinal tract before and after 5 days of treatment. Changes in permeability (lactulose/rhamnose ratio), resulting in increased intestinal permeability caused by indomethacin.
In an in vitro model, the effect of ZnC on cell viability in early (pro-migratory) and late (pro-proliferative) stages of healing was evaluated using human colon cancer cell lines in a lesioned monolayer assay system with serial micrographs. The effect on cell proliferation was assessed by [3H]thymidine incorporation assay using the human intestinal cell lines IEC-6 and HT-29 and the rat intestinal epithelial cell line RIE-1. Indexes of early and late intestinal repair are stimulated. Addition of ZnC to cells resulted in a dose-dependent increase in pro-migratory activity, resulting in a doubling of the wound closure rate. Hyperplasia also increased in a dose-dependent bell-shaped pattern. Likewise, it was shown to protect rat small intestinal epithelial cells from acetyl salicylic acid-induced apoptotic damage by increasing heat shock proteins without negatively affecting the cells.
Drug-induced enterocolitis is caused by numerous morphological and functional changes in the small and large intestines caused by short- or long-term exposure to drugs. This is a very common side effect of many medications. Gastrointestinal disorders and hepatotoxicity are the most common adverse drug reactions that lead to the withdrawal of licensed drugs from the market. Gastrointestinal events such as diarrhea and constipation are the most common gastrointestinal-related adverse drug events and are often associated with the use of nonsteroidal anti-inflammatory drugs (NSAIDs) and antibiotics. In fact, as many as 70% of NSAID users have intestinal mucosal damage, such as lesions, erosions, and even ulcers. It has been suggested that the anti-inflammatory and antioxidant properties of ZnC and its ability to upregulate heat shock proteins may prevent mucosal damage caused by NSAIDs [55]. It was reported that the nuclear factor kappa-light chain enhancer of activated B cells, a pro-inflammatory molecule, was inhibited for 6 hours after administration of ZnC to rats.
A randomized, parallel-group, open-label, controlled, prospective multicenter study was conducted to evaluate the efficacy and safety of ZnC combined with triple therapy (omeprazole 20 mg, amoxicillin 1 g, clarithromycin 500 mg) pylori eradication therapy compared with triple therapy alone. Subjects ( n = 303) were randomly assigned to receive triple therapy plus 75 mg ZnC twice daily, triple therapy plus 150 mg ZnC twice daily, or triple therapy alone. Intention-to-treat (ITT) analysis showed that H. pylori eradication rates were significantly higher in groups A (77.0%) and B (75.9%) compared with group C (58.6%) ( p < 0.01), while groups A and B There were no differences between groups ( p = 0.90). Per-protocol analysis showed that the eradication rate of Helicobacter pylori in Group A (81.1%) and Group B (83.3%) was significantly higher than that in Group C (61.4%) ( p < 0.01), while there was no significant difference between the two groups. Group A and Group B ( p = 0.62). All three groups reported significant improvement in symptoms at 7, 14, and 28 days post-treatment compared with baseline ( p < 0.0001). The incidence of adverse events was higher in Group B (5.1%) than in Group A (2.8%) ( p = 0.04) and Group C (1.9%) ( p = 0.02). There were no serious adverse events in any group. The authors concluded that ZnC is a safe and well-tolerated adjunct to three-in-one therapy for H. pylori eradication . These results are supported by Ko et al., who reported that rats with ulcers given 30 and 60 mg/kg ZnC for 3 consecutive days had a significant reduction in gastric ulcer area in a dose-dependent manner and a corresponding increase in xanthine oxidation content. enzyme and myeloperoxidase activity and malondialdehyde in ulcerated mucosa. Mucosal glutathione was also restored. ZnC also causes overexpression of basic fibroblast growth factor, vascular endothelial growth factor, and ornithine decarboxylase. ZnC consistently downregulates protein expression of activated tumor necrosis factor-α, interleukin-1β, macrophage inflammatory protein-2, and cytokine-induced neutrophil chemoattractant-2α in ulcerated tissue. The authors concluded that ZnC promotes healing effects through its antioxidant effect. Although Handa et al. showed that ZnC may inhibit H. pylori-induced polymorphonuclear leukocyte-mediated gastric inflammation by reducing leukocyte CD11b/CD18 integrin expression and the production of the proinflammatory cytokine interleukin-8 in gastric epithelial cells.
Pressure ulcer
Pressure ulcers (PUs) are a common and costly problem at all levels of healthcare, particularly in bedridden patients, and regardless of initial diagnosis, can be very costly and may reduce outcomes. PU is defined as "localized damage to the skin and/or subcutaneous tissue, usually over bony protrusions, resulting from pressure or a combination of pressure and shear." Guidelines developed by the National Pressure Ulcer Advisory Group and the European Pressure Ulcer Advisory Group recommend that “patients with PU be provided with adequate calories of 30-35 kcal/kg of body weight, adequate protein of 1.25-1.5 g/kg of body weight, and, if deficiencies are present, "Adequate vitamin and mineral supplementation." Despite efforts to follow recommendations and explore different levels of protein, antioxidants, arginine, zinc, and other nutrients, a recent systematic review concluded that nutritional supplementation has no clear benefit. Benefits of the intervention were reported at the time of publication in 2014. However, it has been reported that there is evidence supporting the use of ZnC for the treatment of PU [18, 19]. In a randomized controlled trial, 42 patients with stage II to IV PU were assigned to one of three groups: control ( n = 14 ), oral ZnC 75 mg (58 mg carnosine and 17 mg zinc) ( n = 10) or oral carnosine 58 mg only ( n = 18) for 4 weeks. All other care was identical among the three groups. As assessed by the mean weekly improvement in the Pressure Ulcer Healing Scale (PUSH) score, the carnosine group (1.6 ± 0.2, p = 0.02) and the ZnC group (1.8 ± 0.2, p = 0.009) were better than the control group (0.8 ± 0.2 ). high. The difference between the carnosine group and the ZnC group was not significant ( p = 0.73). The second case series study did not have a control group from the same group, but used comparative data from a previous study, which lasted 8 weeks and included 19 subjects receiving 150 mg ZnC (116 mg carnosine and 34 mg zinc) daily. After 8 weeks, the PUSH score improved significantly from 8.1 [95% CI, 6.0-10.3] at baseline to -1.4 [-4.0 to 1.1] ( p < 0.001). The difference from baseline after 1 week was significant ( p < 0.05). The PUSH score improved by an average of 2.0 per week. Eleven patients recovered within 8 weeks and none dropped out. Serum zinc concentration increased significantly ( p < 0.001). The authors concluded that the data suggest that ZnC may be effective and well tolerated in 8-week treatment of PU. The study also showed a significant decrease in copper levels, which they recommend monitoring in future studies. Although promising, these results are preliminary and warrant future research.
liver
Patients with chronic liver disease have been reported to exhibit impaired trace element metabolism. Specifically, it is high in iron and copper and low in zinc, selenium, phosphorus, calcium and magnesium. Due to its antioxidant and anti-inflammatory effects, zinc supplementation has been hypothesized to be beneficial as an adjunct to chronic hepatitis C treatment. Zinc supplementation has been reported to enhance the response to interferon therapy in patients with refractory chronic hepatitis C.
A significant decrease in serum aminotransferase activity (ALT) was observed in 12 chronic hepatitis C patients supplemented with 150 mg ZnC daily for 48 weeks during combined treatment with PEG-IFN-2b plus ribavirin (n = 12 ) . All patients received 300 mg of vitamin E and 600 mg of vitamin C. ZnC supplementation reduces plasma thiobarbituric acid reactive substances (TBARS) concentrations and prevents a decrease in erythrocyte polyunsaturated fatty acid (PUFA) levels. The authors speculated that ZnC exerted its effect through its antioxidant properties and that PUFA levels were evidence of reduced lipid peroxidation. They believe that because zinc is absorbed in the small intestine and transported to the liver through the portal vein, hepatocytes may be exposed to higher levels of zinc than other tissues, especially during supplementation. The authors concluded that ZnC may provide antioxidant protection in patients with chronic hepatitis undergoing treatment.
A study by Himoto et al. The effects of zinc treatment on liver inflammatory activity and fibrosis in patients with hepatitis C virus (HCV) and chronic liver disease (CLD) were studied. Fourteen patients with HCV-related chronic hepatitis and cirrhosis (defined as persistent elevation of serum aspartate aminotransferase (AST) and/or ALT to more than twice the upper limit of normal for at least 6 months) participated in this study. In addition to prescribed medications, subjects received 75 mg ZnC 3 times/day for 6 months. Peripheral blood counts, serum liver-related biochemical parameters reflecting liver reserve and inflammatory activity, HCV-RNA genotype and burden, serological markers of liver fibrosis (including type IV collagen 7S and hyaluronic acid), and serum levels of trace elements, For example, zinc, copper, iron, and ferritin were examined before and after supplementation. Serum zinc concentration before zinc supplementation was positively correlated with liver reserves. A significant increase in serum zinc concentration was observed after supplementation. Supplementation significantly reduced serum aminotransferase levels and alkaline phosphatase levels. Serum ferritin levels were significantly reduced. The reduction rate of ALT value is positively correlated with the reduction rate of ferritin. There was a downward trend in serum type IV collagen 7S levels after supplementation. However, peripheral blood counts, other liver function tests, or HCV-RNA amounts were not affected. At this supplementation level, copper levels were unaffected, whereas serum ferritin levels were reduced. The authors proposed that ZnC supplementation could reduce liver inflammation in patients with HCV-associated CLD through its antioxidant effects, thereby preventing iron-induced free radical activity.
Nishida et al. It was reported that ZnC and zinc sulfate alone, but not L-carnosine alone, increased HSP70 in primary cultured mouse hepatocytes and prevented acetaminophen toxicity. Cell death and lipid peroxidation were also inhibited. The results indicate that ZnC has a cytoprotective effect, specifically related to the zinc component in hepatocytes experiencing acetaminophen toxicity.
Safety
One potential problem with taking zinc is the potential for copper deficiency, as high doses of zinc are known to inhibit copper absorption. However, a typical dose of ZnC is 22% zinc (and 78% L-carnosine), which usually provides about 15 mg (or 15-16 mg) of zinc, which shouldn't be a problem. Furthermore, ZnC has a long-established safety profile based on long-term use in humans with no reported adverse events and multiple preclinical and human clinical studies.
in conclusion
Taken together, the evidence supports the safety and efficacy of ZnC for the maintenance, prevention, and treatment of mucosal linings and other epithelial tissues. This supports its approval in the United States for use as a dietary zinc supplement and for use in radiation therapy and gastric ulcers, and suggests its other applications, particularly for oral mucositis and dysgeusia in cancer patients undergoing chemoradiotherapy. The anti-inflammatory and antioxidant mechanisms of ZnC further support the reported results regarding efficacy. Further randomized controlled studies in humans are warranted.
