Role of maltol in advanced glycation end products and free radicals: in-vitro and in-vivo studies

2008 ◽  
Vol 60 (4) ◽  
pp. 445-452 ◽  
Author(s):  
Ki Sung Kang ◽  
Noriko Yamabe ◽  
Hyun Young Kim ◽  
Takako Yokozawa
Keyword(s):  
Free Radicals ◽  
Advanced Glycation End Products ◽  
In Vivo Studies ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products

scholarly journals Influence of Dopamine on Fluorescent Advanced Glycation End Products Formation Using Drosophila melanogaster

Biomolecules ◽  
2021 ◽  
Vol 11 (3) ◽  
pp. 453
Author(s):  
Ana Filošević Vujnović ◽  
Katarina Jović ◽  
Emanuel Pištan ◽  
Rozi Andretić Waldowski
Keyword(s):  
Drosophila Melanogaster ◽  
Advanced Glycation End Products ◽  
Model Organism ◽  
Covalent Modification ◽  
Advanced Glycation ◽  
Biomarkers Of Aging ◽  
Glycation End Products ◽  
End Products

Non-enzymatic glycation and covalent modification of proteins leads to Advanced Glycation End products (AGEs). AGEs are biomarkers of aging and neurodegenerative disease, and can be induced by impaired neuronal signaling. The objective of this study was to investigate if manipulation of dopamine (DA) in vitro using the model protein, bovine serum albumin (BSA), and in vivo using the model organism Drosophila melanogaster, influences fluorescent AGEs (fAGEs) formation as an indicator of dopamine-induced oxidation events. DA inhibited fAGEs-BSA synthesis in vitro, suggesting an anti-oxidative effect, which was not observed when flies were fed DA. Feeding flies cocaine and methamphetamine led to increased fAGEs formation. Mutants lacking the dopaminergic transporter or the D1-type showed further elevation of fAGEs accumulation, indicating that the long-term perturbation in DA function leads to higher production of fAGEs. To confirm that DA has oxidative properties in vivo, we fed flies antioxidant quercetin (QUE) together with methamphetamine. QUE significantly decreased methamphetamine-induced fAGEs formation suggesting that the perturbation of DA function in vivo leads to increased oxidation. These findings present arguments for the use of fAGEs as a biomarker of DA-associated neurodegenerative changes and for assessment of antioxidant interventions such as QUE treatment.

scholarly journals Use of Grape Pomace Phenolics to Counteract Endogenous and Exogenous Formation of Advanced Glycation End-Products

Nutrients ◽  
2019 ◽  
Vol 11 (8) ◽  
pp. 1917 ◽  
Author(s):  
Pedapati S. C. Sri Harsha ◽  
Vera Lavelli
Keyword(s):  
Advanced Glycation End Products ◽  
Grape Pomace ◽  
Advanced Glycation ◽  
Sweetened Beverages ◽  
Glycation End Products ◽  
End Products ◽  
Food Applications ◽  
Double Blinded

The increase in consumption of “ultra-processed” foods has raised attention because of the possible adverse effects deriving from the Maillard reaction leading to the formation of toxic advanced glycation end-products (AGEs) during food processing. Additionally, the increasing trend and consumption of sugar-added foods and sweetened beverages is related to the endogenous formation of the same toxic compounds. However, ultra-processing in the context of food technology can bring challenges as well as a wealth of opportunities. Indeed, re-processing of grape pomace, a by-product of winemaking, can yield phenolic-rich fractions that efficiently counteract the effects of AGEs. In this review, the process of endogenous and exogenous AGE formation is illustrated. Then, the ability of grape phenolics to act as inhibitors of AGE formation is presented, including the efficacy ranking of various individual compounds measured in vitro and the outcome of in vivo double-blinded randomized crossover trials designed to prove the efficacy of grape phenolics as inhibitors of protein carbonylation. Finally, a survey of model functional foods added with grape phenolics, either to lower the dietary load of AGEs or to deliver antiglycation agents in vivo is listed in order to highlight the opportunity to develop safe and tailor-made “anti-AGEs” food applications.

scholarly journals Ethyl Pyruvate Prevents Renal Damage Induced by Methylglyoxal-Derived Advanced Glycation End Products

2019 ◽  
Vol 2019 ◽  
pp. 1-9
Author(s):  
Eunsoo Jung ◽  
Wan Seok Kang ◽  
Kyuhyung Jo ◽  
Junghyun Kim
Keyword(s):  
Advanced Glycation End Products ◽  
Ethyl Pyruvate ◽  
Renal Diseases ◽  
Dependent Manner ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products ◽  
Cross Links

The renal accumulation of advanced glycation end products (AGEs) is a causative factor of various renal diseases, including chronic kidney disease and diabetic nephropathy. AGE inhibitors, such as aminoguanidine and pyridoxamine, have the therapeutic activities for reversing the increase in renal AGE burden. This study evaluated the inhibitory effects of ethyl pyruvate (EP) on methylglyoxal- (MGO-) modified AGE cross-links with proteins in vitro. We also determined the potential activity of EP in reducing the renal AGE burden in exogenously MGO-injected rats. EP inhibited MGO-modified AGE-bovine serum albumin (BSA) cross-links to collagen (IC50=0.19±0.03 mM) in a dose-dependent manner, and its activity was stronger than aminoguanidine (IC50=35.97±0.85 mM). In addition, EP directly trapped MGO (IC50=4.41±0.08 mM) in vitro. In exogenous MGO-injected rats, EP suppressed AGE burden and MGO-induced oxidative injury in renal tissues. These activities of EP on the MGO-mediated AGEs cross-links with protein in vitro and in vivo showed its pharmacological potential for inhibiting AGE-induced renal diseases.

scholarly journals Experimental Animal Studies Support the Role of Dietary Advanced Glycation End Products in Health and Disease

Nutrients ◽  
2021 ◽  
Vol 13 (10) ◽  
pp. 3467
Author(s):  
Melpomeni Peppa ◽  
Ioanna Mavroeidi
Keyword(s):  
Diabetes Mellitus ◽  
Experimental Animal ◽  
Advanced Glycation End Products ◽  
Animal Studies ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products ◽  
Health And Disease

The increased incidence of obesity, diabetes mellitus, aging, and associated comorbidities indicates the interplay between genetic and environmental influences. Several dietary components have been identified to play a role in the pathogenesis of the so-called “modern diseases”, and their complications including advanced glycation end products (AGEs), which are generated during the food preparation and processing. Diet-derived advanced glycation end products (dAGEs) can be absorbed in the gastrointestinal system and contribute to the total body AGEs’ homeostasis, partially excreted in the urine, while a significant amount accumulates to various tissues. Various in vitro, in vivo, and clinical studies support that dAGEs play an important role in health and disease, in a similar way to those endogenously formed. Animal studies using wild type, as well as experimental, animal models have shown that dAGEs contribute significantly to the pathogenesis of various diseases and their complications, and are involved in the changes related to the aging process. In addition, they support that dAGEs’ restriction reduces insulin resistance, oxidative stress, and inflammation; restores immune alterations; and prevents or delays the progression of aging, obesity, diabetes mellitus, and their complications. These data can be extrapolated in humans and strongly support that dAGEs’ restriction should be considered as an alternative therapeutic intervention.

scholarly journals Hyperglycemia and advanced glycation end products disrupt BBB and promote occludin and claudin-5 protein secretion on extracellular microvesicles

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Slava Rom ◽  
Nathan A. Heldt ◽  
Sachin Gajghate ◽  
Alecia Seliga ◽  
Nancy L. Reichenbach ◽  
...  
Keyword(s):  
Advanced Glycation End Products ◽  
Connexin 43 ◽  
Ex Vivo ◽  
Advanced Glycation ◽  
Cerebral Microvessels ◽  
Glycation End Products ◽  
End Products ◽  
Bbb Permeability

Abstract Cognitive impairment is a well-known complication of diabetes mellitus (DM). Microvascular compromise was described one DM complication. Recently we showed blood brain barrier (BBB) permeability and memory loss are associated with diminution of tight junctions (TJ) in brain endothelium and pericyte coverage and inflammation in cerebral microvessels and brain tissue paralleling hyperglycemia in mice of both DM types. The current study demonstrates that exposure of brain microvessels to hyperglycemic conditions or advanced glycation end products (AGEs) ex vivo resulted in significant abnormalities in membranous distribution of TJ proteins. We found significant increase in the amount of extracellular vesicles (EVs) isolated from DM mice and enhanced presence of TJ proteins, occludin and claudin-5, on EVs. Exposure of BMVECs to high glucose and AGEs led to significant augmentation of ICAM and VCAM expression, elevated leukocyte adhesion to and migration across BMVEC monolayers, and increased BBB permeability in vitro. Pericytes exposed to hyperglycemia and AGEs displayed diminished expression of integrin α1, PDGF-R1β and connexin-43. Our findings indicate BBB compromise in DM ex vivo, in vitro and in vivo models in association with BMVEC/pericyte dysfunction and inflammation. Prevention of BBB injury may be a new therapeutic approach to avert cognitive demise in DM.

scholarly journals Examining the Role of Dietary Advanced Gycation End Products in Prostate Cancer Using Molecular Imaging Techniques (OR04-08-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Christian Konopka ◽  
Annaliese Paton ◽  
Aleksandra Skokowska ◽  
Joe Rowles ◽  
John Erdman ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Serum Albumin ◽  
Advanced Glycation End Products ◽  
Growth Media ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products ◽  
The Impact

Abstract Objectives The Receptor for Advanced Glycation End Products (RAGE) and its ligands have been shown to be both over expressed and critical to prostate cancer (PCa) development. Importantly, the overexpression of both RAGE and its ligands is associated with poor PCa patient survival, suggesting its promise as a molecular target. Additionally, one of the largest sources of ligands for RAGE, advanced glycation end products (AGEs), come from one's diet and their concentrations are directly related to disease. We hypothesized that dietary AGEs (dAGEs) significantly contribute to the progression of PCa through interactions with RAGE. In this study we explore the use of a novel imaging strategy targeted at RAGE in combination with conventional imaging and histological techniques to assess the role of dAGEs on RAGE expression and PCa progression in murine xenografts. Methods To examine the impact of AGEs on PCa cell function, experiments were performed in two PCa cell lines. Cells were grown in growth media enriched with carboxymethyl-lysine-modified human serum albumin (CML) (the most common AGE) or a control protein, bovine serum albumin (BSA). Western blot, confocal microscopy, clonogenic assays, and proliferations assays were performed. To study the effects of an enhanced consumption of dAGEs on PCa growth and progression in vivo, NU/J mice were fed a modified Ain-93 G diet, which was either CML or BSA enriched. PCa tumors were then initiated. Their growth was monitored, their perfusion measured using Speckle Contrast Imaging, and their metabolic rate and RAGE content quantified using 18FDG and a novel RAGE-targeted tracer using PET-CT. Finally, the tissues were excised for histological analysis. Results CML significantly enhanced in vitro expression of both RAGE and proliferation marker KI-67. Cell doubling time was also significantly quickened, (1.5 vs 2.4 days) in the CML vs control. In vivo data demonstrated significant differences in tumor growth (CML group up to 2-fold increase) and successful tumor implantation rate (30% vs 60%). Perfusion, metabolism, and RAGE imaging demonstrated unique patterns which varied over the course of PCa progression. Conclusions These studies indicate that dAGEs may play a significant role in the progression of PCa. The data suggests that RAGE and its ligands are promising targets for further therapeutic investigations. Funding Sources University of Illinois at Chicago Cancer Center Pilot Grant. Supporting Tables, Images and/or Graphs

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