Depsidic gallotannins and simpler galloylated glucose derivatives all inhibit amyloid β-peptide (Aβ) aggregation in vitro, and monogalloylated α-glucogallin and a natural β-hexagalloylglucose are shown to be the strongest inhibitors.

PMID: 

Angew Chem Int Ed Engl. 2015 Jul 6 ;54(28):8217-21. Epub 2015 May 26. PMID: 26013280

Abstract Title: 

Gallotannins and Tannic Acid: First Chemical Syntheses and In Vitro Inhibitory Activity on Alzheimer's Amyloidβ-Peptide Aggregation.

Abstract: 

The screening of natural products in the search for new lead compounds against Alzheimer's disease has unveiled several plant polyphenols that are capable of inhibiting the formation of toxicβ-amyloid fibrils. Gallic acid based gallotannins are among these polyphenols, but their antifibrillogenic activity has thus far been examined using"tannic acid", a commercial mixture of gallotannins and other galloylated glucopyranoses. The first total syntheses of two true gallotannins, a hexagalloylglucopyranose and a decagalloylated compound whose structure is commonly used to depict"tannic acid", are now described. These depsidic gallotannins and simpler galloylated glucose derivatives all inhibit amyloidβ-peptide (Aβ) aggregation in vitro, and monogalloylated α-glucogallin and a natural β-hexagalloylglucose are shown to be the strongest inhibitors.

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Beta-glucogallin may be a potential drug for the prevention of cataract development and progression.

PMID: 

Med Sci Monit. 2019 Dec 7 ;25:9310-9318. Epub 2019 Dec 7. PMID: 31811113

Abstract Title: 

Protective Effect ofβ-Glucogallin on Damaged Cataract Against Methylglyoxal Induced Oxidative Stress in Cultured Lens Epithelial Cells.

Abstract: 

BACKGROUNDß-glucogallin (GG) is one of the major plant polyphenolic antioxidants that have been associated with positive effects on human health and are crucial in the developing defense mechanism against the risk of diseases. However, reports on the protective mechanism of GG in lens epithelial cells are limited. MATERIAL AND METHODS ARPE-19 cells (a human retinal epithelial cell line) were exposed to methylglyoxal (MG) with or without GG to illuminate the protective role of GG in counteracting the cataract signaling. RESULTS Cells predisposed to MG demonstrated an increase in oxidative stress with augmented (P

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Combination of epigallocatechin gallate and sulforaphane dounteracts In Vitro oxidative stress and delays stemness loss of amniotic fluid stem cells.

PMID: 

Oxid Med Cell Longev. 2018 ;2018:5263985. Epub 2018 Dec 17. PMID: 30647811

Abstract Title: 

Combination of Epigallocatechin Gallate and Sulforaphane Counteracts In Vitro Oxidative Stress and Delays Stemness Loss of Amniotic Fluid Stem Cells.

Abstract: 

Amniotic fluid stem cells (AFSCs) are characterizedby a unique niche guarantying their homeostatic role in the body. Maintaining the functionality of stem cellsfor clinical applications requires a continuous improvement of cell culture conditions. Cellular redox status plays an important role in stem cell biology as long as reactive oxygen species (ROS) concentration is finely regulated and their adverse effects are excluded. The aim of this study was to investigate the protective effect of two antioxidants, sulforaphane (SF) and epigallocatechin gallate (EGCG), againstoxidative stress due to hyperoxia and freeze-thawing cycles in AFSCs. Human AFSCs were isolated and characterized from healthy subjects. Assays of metabolic function and antioxidant activity were performed to investigate the effect of SF and EGCG cotreatment on AFSCs. Real-time PCR was used to investigate the effect of the cotreatment on pluripotency, senescence, osteogenic and adipogenic markers, and antioxidant enzymes. Alkaline phosphatase assays and Alizarin Red staining were used to confirm osteogenic differentiation. The cotreatment with SF and EGCG was effective in reducing ROS production, increasing GSH levels, and enhancing the endogenous antioxidant defences through the upregulation of glutathione reductase, NAD(P)H:quinone oxidoreductase-1, and thioredoxin reductase. Intriguingly, the cotreatment sustained the stemness state by upregulating pluripotency markers such as OCT4 and NANOG. Moreover, the cotreatment influenced senescence-associated gene markers in respect to untreated cells. The cotreatment upregulated osteogenic gene markers and promoted osteogenic differentiation. SF and EGCG can be used in combination in AFSC culture as a strategy to preserve stem cell functionality.

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Whey protein hydrolysate supplementation accelerates recovery from exercise-induced muscle damage in females.

PMID: 

Appl Physiol Nutr Metab. 2018 Apr ;43(4):324-330. Epub 2017 Nov 6. PMID: 29106812

Abstract Title: 

Whey protein hydrolysate supplementation accelerates recovery from exercise-induced muscle damage in females.

Abstract: 

A number of different forms of protein and their analogues have been investigated for their efficacy in ameliorating exercise-induced muscle damage (EIMD) and recovery. Preliminary data regarding whey protein hydrolysate (WPH) supplementation are promising. However, its efficacy beyond acute eccentric/resistance exercise bouts or longer term training programmes are limited and all investigations have been conducted in male or mixed-sex groups. This study sought to elucidate whether the benefits of WPH previously reported can be demonstrated in females following repeated-sprint exercise. Twenty physically active females were assigned to consume 2 doses of 70 mL WPH or isoenergetic carbohydrate (CHO) for 4 days post-EIMD. Measures of muscle soreness, limb girth, flexibility, muscle function, and creatine kinase were collected before, immediately after, and 24, 48, and 72 h postexercise. Time effects were observed for all variables (p

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The effect of whey protein supplementation on the temporal recovery of muscle function following resistance training.

PMID: 

Nutrients. 2018 Feb 16 ;10(2). Epub 2018 Feb 16. PMID: 29462923

Abstract Title: 

The Effect of Whey Protein Supplementation on the Temporal Recovery of Muscle Function Following Resistance Training: A Systematic Review and Meta-Analysis.

Abstract: 

Whey protein (WP) is a widely consumed nutritional supplement, known to enhance strength and muscle mass during resistance training (RT) regimens. Muscle protein anabolism is acutely elevated following RT, which is further enhanced by WP. As a result, there is reason to suggest that WP supplementation may be an effective nutritional strategy for restoring the acute loss of contractile function that occurs following strenuous RT. This systematic review and meta-analysis provides a synthesis of the literature to date, investigating the effect of WP supplementation on the recovery of contractile function in young, healthy adults. Eight studies, containing 13 randomised control trials (RCTs) were included in this review and meta-analysis, from which individual standardised effect sizes (ESs) were calculated, and a temporal overall ES was determined using a random-effects model. Whilst only half of the individual studies reported beneficial effects for WP, the high-quality evidence taken from the 13 RCTs was meta-analysed, yielding overall positive small to medium effects for WP from

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Whey protein supplementation can increase glutathione levels and improve nutritional status and immunity in cancer patients undergoing chemotherapy.

PMID: 

J Med Food. 2018 Jun ;21(6):612-616. Epub 2018 Mar 12. PMID: 29565716

Abstract Title: 

Whey Protein Supplementation Improves Nutritional Status, Glutathione Levels, and Immune Function in Cancer Patients: A Randomized, Double-Blind Controlled Trial.

Abstract: 

Clinical side effects from medical therapy play an important role in causing malnutrition among cancer patients. Whey protein isolates (WPIs) have the potential to improve the nutritional status of cancer patients. The present study determined the effects of whey protein supplementation on nutritional status, glutathione (GSH) levels, immunity, and inflammatory markers in cancer patients in Thailand. A total of 42 cancer patients (41-63 years old) who received intravenous chemotherapy were randomized in a double-blind controlled trial at the National Cancer Institute in Thailand. Patients received 40 g of WPI plus zinc and selenium (intervention group, n = 23) or a maltodextrin oral snack (control group, n = 19) every day during the daytime for 12 weeks. Nutritional status, GSH levels, immunity, and inflammatory markers were assessed at baseline, 6, and 12 weeks. Whey protein supplementation significantly increased albumin (2.9%) and immunoglobulin G (4.8%) levels compared to the control group at week 12. Controls showed a significantly lower percent change in GSH levels (6.0%), whereas there was a significant time-dependent increase in the intervention group (11.7%). Whey protein supplementation improved nutrition status scores in the intervention group compared to the control. These data indicate that whey protein supplementation can increase GSH levels and improve nutritional status and immunity in cancer patients undergoing chemotherapy. These results will facilitate implementation of malnutrition risk prevention strategies and improve protein status, including immune function, during chemotherapy.

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Role of glutathione in cancer progression and chemoresistance.

PMID: 

Oxid Med Cell Longev. 2013 ;2013:972913. Epub 2013 May 20. PMID: 23766865

Abstract Title: 

Role of glutathione in cancer progression and chemoresistance.

Abstract: 

Glutathione (GSH) plays an important role in a multitude of cellular processes, including cell differentiation, proliferation, and apoptosis, and disturbances in GSH homeostasis are involved in the etiology and progression of many human diseases including cancer. While GSH deficiency, or a decrease in the GSH/glutathione disulphide (GSSG) ratio, leads to an increased susceptibility to oxidative stress implicated in the progression of cancer, elevated GSH levels increase the antioxidant capacity and the resistance to oxidative stress as observed in many cancer cells. The present review highlights the role of GSH and related cytoprotective effects in the susceptibility to carcinogenesis and in the sensitivity of tumors to the cytotoxic effects of anticancer agents.

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Ascorbate could serve as a component of a topical antifungal therapy.

PMID: 

Future Microbiol. 2016 12 ;11:1535-1547. Epub 2016 Nov 18. PMID: 27855492

Abstract Title: 

Sodium ascorbate kills Candida albicans in vitro via iron-catalyzed Fenton reaction: importance of oxygenation and metabolism.

Abstract: 

AIM: Ascorbate can inhibit growth and even decrease viability of various microbial species including Candida albicans. However the optimum conditions and the mechanism of action are unclear. Materials/methodology: Candida albicans shaken for 90 min in a buffered solution of ascorbate (90 mM) gave a 5-log reduction of cell viability, while there was no killing without shaking, in growth media with different carbon sources or at 4°C. Killing was inhibited by the iron chelator 2,2'-bipyridyl. Hydroxyphenyl fluorescein probe showed the intracellular generation of hydroxyl radicals.RESULTS/CONCLUSION: Ascorbate-mediated killing of C. albicans depends on oxygenation and metabolism, involves iron-catalyzed generation of hydroxyl radicals via Fenton reaction and depletion of intracellular NADH. Ascorbate could serve as a component of a topical antifungal therapy.

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High doses of sodium ascorbate interfere with the expansion of glioblastoma multiforme cells in vitro and in vivo.

PMID: 

Life Sci. 2019 Sep 1 ;232:116657. Epub 2019 Jul 13. PMID: 31306660

Abstract Title: 

High doses of sodium ascorbate interfere with the expansion of glioblastoma multiforme cells in vitro and in vivo.

Abstract: 

AIMS: Constant development of chemotherapeutic strategies has considerably improved the efficiency of tumor treatment. However, adverse effects of chemotherapeutics enforce premature treatment cessation, which leads to the tumor recurrence and accelerated death of oncologic patients. Recently, sodium ascorbate (ASC) has been suggested as a promising drug for the adjunctive chemotherapy of glioblastoma multiforme (GBM) and prostate cancer (PC). To estimate whether ASC can interfere with tumor recurrence between the first and second-line chemotherapy, we analyzed the effect of high ASC doses on the expansion of cells in vitro and in vivo.MAIN METHODS: Brightfield microscopy-assisted approaches were used to estimate the effect of ASC (1-14 mM) on the morphology and invasiveness of human GBM, rat PC and normal mouse 3T3 cells, whereas cytostatic/pro-apoptotic activity of ASC was estimated with flow cytometry. These assays were complemented by the in vitro CellROX-assisted analyses of intracellular oxidative stress and in vivo estimation of GBM tumor invasion.KEY FINDINGS: ASC considerably decreased the proliferation and motility of GBM and PC cells. This effect was accompanied by intracellular ROS over-production and necrotic death of tumor cells, apparently resulting from their"autoschizis". In vivo studies demonstrated the retardation of GBM tumor growth and invasion in the rats undergone intravenous ASC administration, in the absence of detectable systemic adverse effects of ASC.SIGNIFICANCE: Our data support previous notions on anti-tumor activity of high ASC doses. However, autoschizis-related cell responses to ASC indicate that its application in human adjunctive tumor therapy should be considered with caution.

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Sodium ascorbate as a quorum sensing inhibitor of Pseudomonas aeruginosa.

PMID: 

J Appl Microbiol. 2014 Nov ;117(5):1388-99. Epub 2014 Oct 3. PMID: 25175797

Abstract Title: 

Sodium ascorbate as a quorum sensing inhibitor of Pseudomonas aeruginosa.

Abstract: 

AIMS: Quorum sensing circuits regulate virulence factors in Pseudomonas aeruginosa and coordinate bacterial pathogenicity. We are interested in exploring available medications for their antiquorum sensing activity.METHODS AND RESULTS: First, we determined the MIC of ascorbate against Ps. aeruginosa strain PAO1, and all further experiments used concentrations below the MIC so that results could not be caused by reduced viability. Tests of subinhibitory concentrations of sodium ascorbate on cell signals were performed using a reporter strain assay. Sub-MICs of sodium ascorbate resulted in significant reduction of the signalling molecules C4-HSL and 3-oxo-C12-HSL (P

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