Decreased Formation of Advanced Glycation End-Products in Peritoneal Fluid by Carnosine and Related Peptides

2007 ◽  
Vol 27 (1) ◽  
pp. 86-89 ◽  
Author(s):  
Mohamed-Saiel Saeed Alhamdani ◽  
Hasan Fayadh Al-Azzawie ◽  
Fawzi K.H. Abbas
Keyword(s):  
Advanced Glycation End Products ◽  
Collagen Type Iv ◽  
Advanced Glycation ◽  
Short Term ◽  
Fluorescence Spectrophotometry ◽  
Age Related ◽  
Short Term Exposure ◽  
Glycation End Products ◽  
End Products ◽  
Related Compounds

Background Formation of advanced glycation end-products (AGEs) is a major problem in uremic patients treated with peritoneal dialysis (PD). Application of additives with known anti-glycosylation properties to PD fluid may be beneficial in minimizing the formation of AGEs. This study aimed to evaluate the effect of carnosine and its related peptides homocarnosine and anserine against the formation of AGEs in PD fluid. Methods PD solutions (1.5% dextrose) were incubated with human serum albumin (HSA) or collagen (type IV) with or without 10 mmol/L of each of carnosine, anserine, homo-carnosine, histidine, and aminoguanidine. The formation of AGEs was followed by fluorescence spectrophotometry at weekly intervals for 7 weeks. For the determination of the acute effect of carnosine and related compounds, HSA and collagen were incubated with 4.25% dextrose PD solutions for 24 hours, followed by incubation with 20 mmol/L of carnosine and related compounds for another 24 hours. The rate of AGE formation was monitored by fluorescence spectrophotometry. Results Carnosine and related compounds showed effective regression in AGE formation in both types of proteins in both long- and short-term exposure to PD fluids at a rate of effectiveness of the order of carnosine > homocarnosine > anserine, aminoguanidine > histidine in long-term exposure, and homocarnosine > carnosine > aminoguanidine > anserine > histidine in short-term exposure. Conclusion Carnosine and related peptides could suppress the formation of AGEs initiated by PD fluid. This observation may provide a new therapeutic approach for the prevention and treatment of the AGE-related complications in PD patients.

Short-Term Low Calorie Diet Intervention Reduces Serum Advanced Glycation End Products in Healthy Overweight or Obese Adults

2009 ◽  
Vol 54 (3) ◽  
pp. 197-201 ◽  
Author(s):  
Alejandro Gugliucci ◽  
Kazuhiko Kotani ◽  
Jennifer Taing ◽  
Yukiyo Matsuoka ◽  
Yoshiko Sano ◽  
...  
Keyword(s):  
Advanced Glycation End Products ◽  
Advanced Glycation ◽  
Short Term ◽  
Obese Adults ◽  
Low Calorie ◽  
Diet Intervention ◽  
Low Calorie Diet ◽  
Glycation End Products ◽  
End Products ◽  
Calorie Diet

Dietary sugars and related endogenous advanced glycation end-products increase chromosomal DNA damage in WIL2-NS cells, measured using cytokinesis-block micronucleus cytome assay

Mutagenesis ◽  
2020 ◽  
Vol 35 (2) ◽  
pp. 169-177 ◽  
Author(s):  
Permal Deo ◽  
Caitlin L McCullough ◽  
Theodora Almond ◽  
Emma L Jaunay ◽  
Leigh Donnellan ◽  
...  
Keyword(s):  
Dna Damage ◽  
Advanced Glycation End Products ◽  
Chromosomal Dna ◽  
Advanced Glycation ◽  
Age Related ◽  
Genome Damage ◽  
Glycation End Products ◽  
End Products ◽  
High Concentrations

Abstract This study investigated the effect of glucose and fructose, and advanced glycation end-products (AGEs) on genome damage in WIL2-NS cells, measured using the cytokinesis-block micronucleus cytome (CBMN-Cyt) assay. The effect of AGEs was investigated using the bovine serum albumin (AGE-BSA) model system induced either with glucose (Glu–BSA) or with fructose (Fru–BSA). Liquid chromatography-mass spectrometry (LC-MS/MS) analysis showed higher Nε-carboxymethyllysine (CML; 26.76 ± 1.09 nmol/mg BSA) levels in the Glu–BSA model. Nε-Carboxyethyllysine (CEL; 7.87 ± 0.19 nmol/mg BSA) and methylglyoxal-derived hydroimidazolone-1 (MG-H1; 69.77 ± 3.74 nmol/mg BSA) levels were higher in the Fru–BSA model. Genotoxic effects were measured using CBMN-Cyt assay biomarkers [binucleated(BN) cells with micronuclei (MNi), BN with nucleoplasmic bridges (NPBs) and BN with nuclear buds (NBuds)] following 9 days of treatment with either glucose, fructose, Glu–BSA or Fru–BSA. Fructose treatment exerted a significant genotoxic dose–response effect including increases of BN with MNi (R2 = 0.7704; P = 0.0031), BN with NPBs (R2 = 0.9311; P < 0.0001) and BN with NBuds (R2 = 0.7118; P = 0.0091) on cells, whereas the DNA damaging effects of glucose were less evident. High concentrations of AGEs (400–600 µg/ml) induced DNA damage; however, there was no effect on cytotoxicity indices (necrosis and apoptosis). In conclusion, this study demonstrates a potential link between physiologically high concentrations of reducing sugars or AGEs with increased chromosomal damage which is an important emerging aspect of the pathology that may be induced by diabetes. Ultimately, loss of genome integrity could accelerate the rate of ageing and increase the risk of age-related diseases over the long term. These findings indicate the need for further research on the effects of glycation on chromosomal instability and to establish whether this effect is replicated in humans in vivo.

scholarly journals The association between dietary and skin advanced glycation end products: the Rotterdam Study

2020 ◽  
Vol 112 (1) ◽  
pp. 129-137 ◽  
Author(s):  
Jinluan Chen ◽  
Komal Waqas ◽  
Robby Carlo Tan ◽  
Trudy Voortman ◽  
M Arfan Ikram ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Advanced Glycation End Products ◽  
Time Difference ◽  
European Ancestry ◽  
Rotterdam Study ◽  
Advanced Glycation ◽  
Age Related ◽  
Glycation End Products ◽  
End Products

ABSTRACT Background Advanced glycation end products (AGEs) accumulate in tissues with age and in conditions such as diabetes mellitus and chronic kidney disease (CKD), and they may be involved in age-related diseases. Skin AGEs measured as skin autofluorescence (SAF) are a noninvasive reflection of long-term AGE accumulation in tissues. Whether AGEs present in the diet (dAGEs) contribute to tissue AGEs is unclear. Objectives Our aim was to investigate the association between dietary and skin AGEs in the Rotterdam Study, a population-based cohort of mainly European ancestry. Methods In 2515 participants, intake of 3 dAGEs [carboxymethyl-lysine (CML), N-(5-hydro-5-methyl-4-imidazolon-2-yl)-ornithine (MGH1), and carboxyethyl-lysine (CEL)] was estimated using FFQs and the content of AGEs measured in commonly consumed foods. SAF was measured 5 y (median value) later using an AGE Reader. The association of dAGEs with SAF was analyzed in linear regression models and stratified for diabetes and chronic kidney disease (CKD, defined as estimated glomerular filtration rate ≤60 mL/min) status. Results Mean ± SD intake was 3.40 ±0.89 mg/d for CML, 28.98 ±7.87 mg/d for MGH1, and 3.11 ±0.89 mg/d for CEL. None of them was associated with SAF in the total study population. However, in stratified analyses, CML was positively associated with SAF after excluding both individuals with diabetes and individuals with CKD: 1 SD higher daily CML intake was associated with a 0.03 (95% CI: 0.009, 0.05) arbitrary units higher SAF. MGH1 and CEL intake were not significantly associated with SAF. Nevertheless, the associations were stronger when the time difference between dAGEs and SAF measurements was shorter. Conclusions Higher dietary CML intake was associated with higher SAF only among participants with neither diabetes nor CKD, which may be explained by high AGE formation in diabetes and decreased excretion in CKD or by dietary modifications in these disease groups. The dAGE–SAF associations were also modified by the time difference between measurements. Our results suggest that dAGEs can influence tissue AGE accumulation and possibly thereby age-related diseases. This trial was registered at the Netherlands National Trial Register as NTR6831 (http://www.trialregister.nl/trialreg/admin/rctview.asp?TC=6831) and at the WHO International Clinical Trials Registry Platform as NTR6831 (http://www.who.int/ictrp/network/primary/en/).

scholarly journals Global proteomic analysis of advanced glycation end products in theArabidopsisproteome provides evidence for age-related glycation hot spots

2017 ◽  
Vol 292 (38) ◽  
pp. 15758-15776 ◽  
Author(s):  
Tatiana Bilova ◽  
Gagan Paudel ◽  
Nikita Shilyaev ◽  
Rico Schmidt ◽  
Dominic Brauch ◽  
...  
Keyword(s):  
Advanced Glycation End Products ◽  
Hot Spots ◽  
Proteomic Analysis ◽  
Advanced Glycation ◽  
Age Related ◽  
Glycation End Products ◽  
End Products

Receptor for Advanced Glycation End Products and Age-Related Macular Degeneration

2004 ◽  
Vol 45 (10) ◽  
pp. 3713 ◽  
Author(s):  
Kimberly A. Howes ◽  
Yang Liu ◽  
Joshua L. Dunaief ◽  
Ann Milam ◽  
Jeanne M. Frederick ◽  
...  
Keyword(s):  
Macular Degeneration ◽  
Advanced Glycation End Products ◽  
Age Related Macular Degeneration ◽  
Advanced Glycation ◽  
Age Related ◽  
Glycation End Products ◽  
End Products

scholarly journals Role of Advanced Glycation End Products in Carcinogenesis and their Therapeutic Implications

2019 ◽  
Vol 24 (44) ◽  
pp. 5245-5251 ◽  
Author(s):  
David Schröter ◽  
Annika Höhn
Keyword(s):  
Advanced Glycation End Products ◽  
Molecular Mechanisms ◽  
The Body ◽  
Advanced Glycation ◽  
Therapeutic Implications ◽  
Age Related ◽  
Glycation End Products ◽  
End Products ◽  
Reduction Strategies

Aging is one of the biggest risk factors for the major prevalent diseases such as cardiovascular diseases, neurodegeneration and cancer, but due to the complex and multifactorial nature of the aging process, the molecular mechanisms underlying age-related diseases are not yet fully understood. Research has been intensive in the last years aiming to characterize the pathophysiology of aging and develop therapies to fight age-related diseases. In this context advanced glycation end products (AGEs) have received attention. AGEs, when accumulated in tissues, significantly increase the level of inflammation in the body which has long been associated with the development of cancer. Here we discuss the classical settings promoting AGE formation, as well as reduction strategies, occurrence and relevance of AGEs in cancer tissues and the role of AGE-interaction with the receptor for advanced glycation end products (RAGE) in cancer initiation and progression.

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