scholarly journals Advanced Glycation End Products Increase Salivary Gland Hypofunction in d-Galactose-Induced Aging Rats and Its Prevention by Physical Exercise

2021 ◽  
Vol 43 (3) ◽  
pp. 2059-2067
Author(s):  
Woo Kwon Jung ◽  
Su-Bin Park ◽  
Hyung Rae Kim ◽  
Hwa Young Ryu ◽  
Yong Hwan Kim ◽  
...  
Keyword(s):  
Salivary Gland ◽  
Physical Exercise ◽  
Advanced Glycation End Products ◽  
Aging Process ◽  
Advanced Glycation ◽  
Young Control ◽  
Aging Rats ◽  
Age Related ◽  
Glycation End Products ◽  
End Products

A declined salivary gland function is commonly observed in elderly people. Advanced glycation end products (AGEs) are believed to contribute to the pathogenesis of aging. Although physical exercise is shown to increase various organ functions in human and experimental models, it is not known whether it has a similar effect in the salivary glands. In the present study, we evaluated the AGEs burden in the salivary gland in the aging process and the protective effect of physical exercise on age-related salivary hypofunction. To accelerate the aging process, rats were peritoneally injected with D-galactose for 6 weeks. Young control rats and d-galactose-induced aging rats in the old group were not exercised. The rats in the physical exercise group ran on a treadmill (12 m/min, 60 min/day, 3 days/week for 6 weeks). The results showed that the salivary flow rate and total protein levels in the saliva of the d-galactose-induced aging rats were reduced compared to those of the young control rats. Circulating AGEs in serum and secreted AGEs in saliva increased with d-galactose-induced aging. AGEs also accumulated in the salivary glands of these aging rats. The salivary gland of aging rats showed increased reactive oxygen species (ROS) generation, loss of acinar cells, and apoptosis compared to young control mice. However, physical exercise suppressed all of these age-related salivary changes. Overall, physical exercise could provide a beneficial option for age-related salivary hypofunction.

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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