Effect of fatty acids and triglycerides on the formation of lysine-derived advanced glycation end-products in model systems exposed to frying temperature

AbstractProtein glycation is initiated by a nucleophilic addition reaction between the free amino group from a protein, lipid or nucleic acid and the carbonyl group of a reducing sugar. This reaction forms a reversible Schiff base, which rearranges over a period of days to produce ketoamine or Amadori products. The Amadori products undergo dehydration and rearrangements and develop a cross-link between adjacent proteins, giving rise to protein aggregation or advanced glycation end products (AGEs). A number of studies have shown that glycation induces the formation of the β-sheet structure in β-amyloid protein, α-synuclein, transthyretin (TTR), copper-zinc superoxide dismutase 1 (Cu, Zn-SOD-1), and prion protein. Aggregation of the β-sheet structure in each case creates fibrillar structures, respectively causing Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, familial amyloid polyneuropathy, and prion disease. It has been suggested that oligomeric species of glycated α-synuclein and prion are more toxic than fibrils. This review focuses on the pathway of AGE formation, the synthesis of different types of AGE, and the molecular mechanisms by which glycation causes various types of neurodegenerative disease. It discusses several new therapeutic approaches that have been applied to treat these devastating disorders, including the use of various synthetic and naturally occurring inhibitors. Modulation of the AGE-RAGE axis is now considered promising in the prevention of neurodegenerative diseases. Additionally, the review covers several defense enzymes and proteins in the human body that are important anti-glycating systems acting to prevent the development of neurodegenerative diseases.

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Induction of 1,2-Dicarbonyl Compounds, Intermediates in the Formation of Advanced Glycation End-Products, during Heat-Sterilization of Glucose-Based Peritoneal Dialysis Fluids

Peritoneal Dialysis International ◽

10.1177/089686089901900408 ◽

1999 ◽

Vol 19 (4) ◽

pp. 325-333 ◽

Cited By ~ 78

Author(s):

Casper G. Schalkwijk ◽

Nynke Posthuma ◽

Herman J. Ten Brink ◽

Pieter M. Ter Wee ◽

Tom Teerlink

Keyword(s):

Peritoneal Dialysis ◽

Advanced Glycation End Products ◽

Dwell Time ◽

Advanced Glycation ◽

Fluorescence Excitation ◽

Dicarbonyl Compounds ◽

Glycation End Products ◽

End Products

Objective To study the presence of 1,2-dicarbonyl compounds in peritoneal dialysis (PD) fluids, their concentration in effluents with increasing dwell time, and their role in the formation of advanced glycation end-products (AGEs). Measurements Dicarbonyl compounds in heat- and filter-sterilized PD fluids were quantified by reverse-phase high performance liquid chromatography (HPLC) after derivatization to dimethoxyquinoxaline derivatives. Kinetics of the in vitro formation of AGEs upon incubation of 1,2-dicarbonyl compounds or PD fluids with albumin, with or without aminoguanidine, were measured by AGE fluorescence (excitation/emission wavelengths of 350 nm/430 nm). Patients AGEs and dicarbonyl compounds were measured in effluents collected from standardized 4-hour dwells from 8 continuous cycling peritoneal dialysis patients. Results In PD fluids, 3-deoxyglucosone (3-DG) has been identified as the major dicarbonyl compound formed during the process of heat sterilization. The process also formed glyoxal (GO) and methylglyoxal (MGO), with the amount of 3-DG being approximately 25 – 60 times higher than GO and MGO. When incubated with albumin, the identified 1,2-dicarbonyl compounds rapidly formed AGEs. The formation of AGEs was more pronounced in conventional heat-sterilized PD fluids compared with filter-sterilized PD fluids, and was completely inhibited by aminoguanidine. In effluents, the concentration of MGO, GO, and 3-DG decreased with increasing dwell time, with a concomitant increase in AGE fluorescence. Conclusions The dicarbonyl compounds 3-DG, MGO, and GO are potent promoters of AGE formation. The presence of these and possibly other dicarbonyl compounds formed during heat sterilization of glucose-based PD fluids is, to a large extent, responsible for the in vitro AGE formation by these fluids, as evidenced by the speed of AGE formation in PD fluids and the complete inhibition by aminoguanidine. Because 3-DG, MGO, and GO are rapidly cleared from PD fluids during dialysis, these compounds may contribute to the in vivo AGE formation in PD patients.

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Comprehensive Analyses of Carbohydrates, 1,2-Dicarbonyl Compounds, and Advanced Glycation End Products in Industrial Bread Making

Journal of Agricultural and Food Chemistry ◽

10.1021/acs.jafc.0c07614 ◽

2021 ◽

Author(s):

Tobias Jost ◽

Christian Henning ◽

Thomas Heymann ◽

Marcus A. Glomb

Keyword(s):

Advanced Glycation End Products ◽

Advanced Glycation ◽

Bread Making ◽

Dicarbonyl Compounds ◽

Glycation End Products ◽

End Products

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Inhibition of the Maillard Reaction by Phytochemicals Composing an Aqueous Coffee Silverskin Extract via a Mixed Mechanism of Action

Foods ◽

10.3390/foods8100438 ◽

2019 ◽

Vol 8 (10) ◽

pp. 438 ◽

Cited By ~ 3

Author(s):

Miguel Rebollo-Hernanz ◽

Beatriz Fernández-Gómez ◽

Miguel Herrero ◽

Yolanda Aguilera ◽

María A. Martín-Cabrejas ◽

...

Keyword(s):

Advanced Glycation End Products ◽

Protein Complexes ◽

Early Stage ◽

In Silico Analysis ◽

Model Systems ◽

Protein Glycation ◽

Advanced Glycation ◽

Coffee Silverskin ◽

Glycation End Products ◽

End Products

This work aimed to evaluate the contribution of isoflavones and melatonin to the aqueous extract obtained from the coffee silverskin (CSE) antiglycative properties, which has not been previously studied. To achieve this goal, two model systems constituted by bovine serum albumin (BSA) and reactive carbonyls (glucose or methylglyoxal) in the presence or absence of pure phytochemicals (chlorogenic acid (CGA), genistein, and melatonin) and CSE were employed. Glucose was used to evaluate the effect on the formation of glycation products formed mainly in the early stage of the reaction, while methylglyoxal was employed for looking at the formation of advanced products of the reaction, also called methylglyoxal-derivative advanced glycation end products (AGE) or glycoxidation products. CGA inhibited the formation of fructosamine, while genistein and melatonin inhibited the formation of advanced glycation end products and protein glycoxidation. It was also observed that phenolic compounds from CSE inhibited protein glycation and glycoxidation by forming BSA–phytochemical complexes. CSE showed a significant antiglycative effect (p < 0.05). Variations in the UV-Vis spectrum and the antioxidant capacity of protein fractions suggested the formation of protein–phytochemical complexes. Fluorescence quenching and in silico analysis supported the formation of antioxidant–protein complexes. For the first time, we illustrate that isoflavones and melatonin may contribute to the antiglycative/antiglycoxidative properties associated with CSE. CGA, isoflavones, and melatonin composing CSE seem to act simultaneously by different mechanisms of action.

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Επιπτώσεις των μεταβολικών διαταραχών και των γλυκοτοξινών στο αναπαραγωγικό σύστημα αρρένων μυών και επίμυων

10.12681/eadd/42406 ◽

2014 ◽

Author(s):

Δημήτριος Μοσχονάς

Keyword(s):

Fatty Acids ◽

Advanced Glycation End Products ◽

Saturated Fatty Acids ◽

Monounsaturated Fatty Acids ◽

Advanced Glycation ◽

Glycation End Products ◽

End Products

Η παχυσαρκία αποτελεί συστηματική διαταραχή με επιπτώσεις σε διάφορα όργανα μεταξύ των οποίων και το ουροποιογεννητικό σύστημα. Η υπεργλυκαιμία, η υπερλιπιδαιμία και το οξειδωτικό stress, στα πλαίσια της παχυσαρκίας οδηγούν στο σχηματισμό τοξικών μεταβολικών προϊόντων, των τελικών προϊόντων προχωρημένης γλυκοζυλίωσης (advanced glycation end products - AGEs), που εναποτίθενται στους ιστούς με βλαπτικές επιδράσεις. Η εξωγενής πρόσληψη και η ενδογενής συσσώρευση συμβάλλουν στην παθογένεια μεταβολικών και αναπαραγωγικών διαταραχών τόσο σε άνδρες όσο και σε γυναίκες. Η παρούσα μελέτη αξιολόγησε την επίδραση διατροφής υψηλής περιεκτικότητας σε κορεσμένα λιπαρά οξέα [saturated fatty acids (SAFA)] στο λιπιδαιμικό και μεταβολικό προφίλ (επίπεδα AGE, οξειδωτικό stress) καθώς επίσης και στις ιστοπαθολογικές (έκφραση AGE, RAGE, απόπτωση) και μορφομετρικές παραμέτρους του αναπαραγωγικού συστήματος αρρένων μυών C57BL6 in vivo. Μετά την εκδήλωση παχυσαρκίας τα αποτελέσματα της χορήγησης διατροφής πλούσιας σε μονοακόρεστα λιπαρά οξέα [monounsaturated fatty acids (MUFA)] ή ίσης περιεκτικότητας MUFA και SAFA εκτιμήθηκαν. Τα πειραματόζωα της ομάδας SAFA παρουσίασαν υψηλές συγκεντρώσεις χοληστερόλης (p < .05) σε σύγκριση με τους μάρτυρες, ενώ τα επίπεδα AGE και υπεροξειδίων δεν διέφεραν στατιστικά σημαντικά μεταξύ των διαφόρων ομάδων πειραματισμού. Αυξημένη εναπόθεση AGE ανιχνεύθηκε για πρώτη φορά στα γαμετικά κύτταρα με υψηλότερη ένταση χρώσης σε ζώα με υψηλή σε SAFA διατροφή, σε σύγκριση με τη MUFA ή MUFA-SAFA τροφή ή τους μάρτυρες (p = .018). Στα κύτταρα Leydig, η εντόπιση AGE ήταν υψηλότερη στην ομάδα πειραματοζώων με τροφή υψηλή σε λιπαρά σε σύγκριση με τους μάρτυρες (p < .05). Επίσης παρουσιάζουν αυξημένο αποπτωτικό δείκτη στα σπερματικά τους κύτταρα (p < .005). Επιπλέον παρατηρήθηκε μείωση της πτύχωσης του βλεννογόνου του προστάτη των ζώων, η οποία αντιστράφηκε μετά τη χορήγηση της τροφής MUFA. Τα αποτελέσματα αυτά αποτελούν το έναυσμα για περαιτέρω διερεύνηση του ρόλου του άξονα AGE–RAGE σε διαταραχές των όρχεων και του προστάτη στα πλαίσια της προκαλούμενης από τη διατροφή παχυσαρκίας. Απλές διατροφικές παρεμβάσεις θα μπορούσαν να έχουν ευεργετική επίδραση στη μεταβολική δυσλειτουργία του αναπαραγωγικού συστήματος πριν την εκδήλωση συστηματικών μεταβολικών διαταραχών, υποδεικνύοντας τη γλυκοζυλίωση ως υποσχόμενο θεραπευτικό στόχο.

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