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  1. Mbous YP, Hayyan M, Wong WF, Looi CY, Hashim MA
    Sci Rep, 2017 02 01;7:41257.
    PMID: 28145498 DOI: 10.1038/srep41257
    In this study, the anticancer potential and cytotoxicity of natural deep eutectic solvents (NADESs) were assessed using HelaS3, PC3, A375, AGS, MCF-7, and WRL-68 hepatic cell lines. NADESs were prepared from choline chloride, fructose, or glucose and compared with an N,N-diethyl ethanolammonium chloride:triethylene glycol DES. The NADESs (98 ≤ EC50 ≥ 516 mM) were less toxic than the DES (34 ≤ EC50 ≥ 120 mM). The EC50 values of the NADESs were significantly higher than those of the aqueous solutions of their individual components but were similar to those of the aqueous solutions of combinations of their chief elements. Due to the uniqueness of these results, the possibility that NADESs could be synthesized intracellularly to counterbalance the cytotoxicity of their excess principal constituents must be entertained. However, further research is needed to explore this avenue. NADESs exerted cytotoxicity by increasing membrane porosity and redox stress. In vivo, they were more destructive than the DES and induced liver failure. The potential of these mixtures was evidenced by their anticancer activity and intracellular processing. This infers that they can serve as tools for increasing our understanding of cell physiology and metabolism. It is likely that we only have begun to comprehend the nature of NADESs.
    Matched MeSH terms: Glycosylation End Products, Advanced/metabolism
  2. Angelopoulou E, Paudel YN, Piperi C
    ACS Chem Neurosci, 2020 03 04;11(5):663-673.
    PMID: 32017530 DOI: 10.1021/acschemneuro.9b00678
    Myasthenia gravis (MG) is an autoimmune T cell-dependent B cell-mediated disorder of the neuromuscular junction (NMJ) characterized by fluctuating skeletal muscle weakness, most commonly attributed to pathogenic autoantibodies against postsynaptic nicotinic acetylcholine receptors (AChRs). Although MG pathogenesis is well-documented, there are no objective biomarkers that could effectively correlate with disease severity or MG clinical subtypes, and current treatment approaches are often ineffective. The receptor for advanced glycation end products (RAGE) is a multiligand cell-bound receptor highly implicated in proinflammatory responses and autoimmunity. Preclinical evidence demonstrates that RAGE and its ligand S100B are upregulated in rat models of experimental autoimmune myasthenia gravis (EAMG). S100B-mediated RAGE activation has been shown to exacerbate EAMG, by enhancing T cell proinflammatory responses, aggravating T helper (Th) subset imbalance, increasing AChR-specific T cell proliferative capacity, and promoting the production of antibodies against AChRs from the spleen. Soluble sRAGE and esRAGE, acting as decoys of RAGE ligands, are found to be significantly reduced in MG patients. Moreover, MG has been associated with increased serum levels of S100A12, S100B and HMGB1. Several studies have shown that the presence of thymic abnormalities, the onset age of MG, and the duration of the disease may affect the levels of these proteins in MG patients. Herein, we discuss the emerging role of RAGE and its ligands in MG immunopathogenesis, their clinical significance as promising biomarkers, as well as the potential therapeutic implications of targeting RAGE signaling in MG treatment.
    Matched MeSH terms: Glycosylation End Products, Advanced
  3. Hua Z, Wang S, Yuan X
    J Affect Disord, 2024 Apr 01;350:831-837.
    PMID: 38242215 DOI: 10.1016/j.jad.2024.01.009
    BACKGROUND: The objective of this study was to provide a comprehensive analysis of the spatial distribution and temporal trends in the age-standardized incidence rates (ASIRs) of depression in adolescents aged 10-24 worldwide.

    METHODS: Data from the Global Burden of Disease Study (GBD) 2019 were analyzed, adopting Sawyer's broad definition of adolescence encompassing ages 10 to 24. Estimated annual percentage changes (EAPCs) were used to assess temporal trends.

    RESULTS: Globally, from 1990 to 2019, there was a decrease in the ASIR of depression in adolescents (EAPC = -0.23). Notably, this decrease was more pronounced in female adolescents compared to their male counterparts (EAPC = -0.12 and - 0.29, respectively). Conversely, high Sociodemographic Index (SDI) regions experienced a significant increase in the ASIR of depression among adolescents (EAPC = 0.87). Furthermore, it is worth mentioning that individuals aged 20-24 exhibited the highest incidence rate for depression followed by those aged 15-19 and then those aged 10-14. The largest increases in the ASIRs of depression occurred in High-income North America (EAPC = 1.19) and Malaysia (EAPC = 2.4), respectively.

    LIMITATIONS: Mathematical models were used to reconstruct and adjust data of different qualities, which might have introduced bias.

    CONCLUSIONS: The global burden of disease for depression among adolescents aged 10-24 years declined from 1990 to 2019. Special attention must be paid to older adolescents and areas with higher SDIs.

    Matched MeSH terms: Glycosylation End Products, Advanced*
  4. Norlinah MI, Hamizah R, Md Isa SH, Wan Nazaimoon WM, Khalid BA
    Indian J Med Sci, 2009 Apr;63(4):131-8.
    PMID: 19414982
    BACKGROUND: The role of endothelial injury and circulating adhesion molecule in the development and progression of diabetic peripheral neuropathy in the long-term has been established previously.
    AIMS: To study the effects of short-term glycemic control using insulin and oral hypoglycemic agent therapy (OHA) on the peroneal nerve function and vascular cell adhesion molecule-1 (VCAM-1) and advanced glycation endproducts (AGE) levels in type 2 diabetic patients.
    SETTINGS AND DESIGN: A randomized controlled study involving poorly controlled (HbA1c, 7.5%-11%) type 2 diabetic patients attending the endocrinology outpatient center in a tertiary hospital in Kuala Lumpur.
    MATERIALS AND METHODS: Twenty-nine patients were randomized to receive insulin (n=15) or OHA (n=14) for 8 weeks. The glycemic variables (HbA1c, fasting plasma glucose [FPG], fructosamine), VCAM-1, serum AGE and the peroneal motor conduction velocity (PMCV) were measured at baseline and at 4-week intervals.
    STATISTICAL ANALYSIS USED: Paired 't' test or Kruskal Wallis test; and the unpaired 't' test or Mann-Whitney U test were used for within-group and between-group analyses, respectively. Correlation was analyzed using Spearman's correlation coefficient.
    RESULTS: Within-group analysis showed significant progressive improvement in HbA1c at weeks 4 and 8 in the insulin group. The PMCV improved significantly in both groups by week 8, and by week 4 (P = 0.01) in the insulin group. PMCV correlated negatively with VCAM-1 (P = 0.031) and AGE (P = 0.009) at week 8.
    CONCLUSION: Aggressive glycemic control with insulin improves the peroneal nerve function within 4 weeks. Improvement in the serum VCAM-1 and AGE levels correlated significantly with improvement in peroneal nerve conduction velocity only in the insulin group.
    Study site: Tertiary endocrinology outpatient center in Kuala Lumpur, Malaysia
    Matched MeSH terms: Glycosylation End Products, Advanced/blood
  5. Kong SY, Takeuchi M, Hyogo H, McKeown-Eyssen G, Yamagishi S, Chayama K, et al.
    Cancer Epidemiol Biomarkers Prev, 2015 Dec;24(12):1855-63.
    PMID: 26404963 DOI: 10.1158/1055-9965.EPI-15-0422
    BACKGROUND: A large proportion of colorectal cancers are thought to be associated with unhealthy dietary and lifestyle exposures, particularly energy excess, obesity, hyperinsulinemia, and hyperglycemia. It has been suggested that these processes stimulate the production of toxic reactive carbonyls from sugars such as glyceraldehyde. Glyceraldehyde contributes to the production of a group of compounds known as glyceraldehyde-derived advanced glycation end-products (glycer-AGEs), which may promote colorectal cancer through their proinflammatory and pro-oxidative properties. The objective of this study nested within a prospective cohort was to explore the association of circulating glycer-AGEs with risk of colorectal cancer.

    METHODS: A total of 1,055 colorectal cancer cases (colon n = 659; rectal n = 396) were matchced (1:1) to control subjects. Circulating glycer-AGEs were measured by a competitive ELISA. Multivariable conditional logistic regression models were used to calculate ORs and 95% confidence intervals (95% CI), adjusting for potential confounding factors, including smoking, alcohol, physical activity, body mass index, and diabetes status.

    RESULTS: Elevated glycer-AGEs levels were not associated with colorectal cancer risk (highest vs. lowest quartile, 1.10; 95% CI, 0.82-1.49). Subgroup analyses showed possible divergence by anatomical subsites (OR for colon cancer, 0.83; 95% CI, 0.57-1.22; OR for rectal cancer, 1.90; 95% CI, 1.14-3.19; Pheterogeneity = 0.14).

    CONCLUSIONS: In this prospective study, circulating glycer-AGEs were not associated with risk of colon cancer, but showed a positive association with the risk of rectal cancer.

    IMPACT: Further research is needed to clarify the role of toxic products of carbohydrate metabolism and energy excess in colorectal cancer development.

    Matched MeSH terms: Glycosylation End Products, Advanced/blood*
  6. Cheng HS, Ton SH, Tan JBL, Abdul Kadir K
    Nutrients, 2017 Sep 07;9(9).
    PMID: 28880217 DOI: 10.3390/nu9090984
    The clinical value of tocotrienols is increasingly appreciated because of the unique therapeutic effects that are not shared by tocopherols. However, their effect on metabolic syndrome is not well-established. This study aimed to investigate the effects of a tocotrienol-rich fraction (TRF) from palm oil in high-fat-diet-treated rats. Male, post-weaning Sprague Dawley rats were provided high-fat (60% kcal) diet for eight weeks followed by a TRF (60 mg/kg) treatment for another four weeks. Physical, metabolic, and histological changes were compared to those on control and high-fat diets respectively. High-fat feeding for eight weeks induced all hallmarks of metabolic syndrome. The TRF reversed systolic and diastolic hypertension, hypercholesterolemia, hepatic steatosis, impaired antioxidant defense, and myeloperoxidase hyperactivity triggered by the high-fat diet. It also conferred an inhibitory effect on protein glycation to reduce glycated hemoglobin A1c and advanced glycation end products (AGE). This was accompanied by the suppression of the receptor for advanced glycation end product (RAGE) expression in the liver. The treatment effects on visceral adiposity, glycemic control, triglyceride level, as well as peroxisome proliferator-activated receptor α and γ expression were negligible. To conclude, treatment with a TRF exhibited protective effects on the cardiovascular and liver health in addition to the amelioration of plasma redox imbalance and AGE-RAGE activation. Further investigation as a therapy for metabolic syndrome is therefore worthwhile.
    Matched MeSH terms: Glycosylation End Products, Advanced/metabolism*
  7. Dong L, Li Y, Chen Q, Liu Y, Qiao Z, Sang S, et al.
    Food Chem, 2023 Aug 15;417:135861.
    PMID: 36906946 DOI: 10.1016/j.foodchem.2023.135861
    Advanced glycosylation end products (AGEs) are a series of complex compounds which generate in the advanced phase of Maillard reaction, which can pose a non-negligible risk to human health. This article systematically encompasses AGEs in milk and dairy products under different processing conditions, influencing factors, inhibition mechanism and levels among the different categories of dairy products. In particular, it describes the effects of various sterilization techniques on the Maillard reaction. Different processing techniques have a significant effect on AGEs content. In addition, it clearly articulates the determination methods of AGEs and even discusses its immunometabolism via gut microbiota. It is observed that the metabolism of AGEs can affect the composition of the gut microbiota, which further has an impact on intestinal function and the gut-brain axis. This research also provides a suggestion for AGEs mitigation strategies, which are beneficial to optimize the dairy production, especially innovative processing technology application.
    Matched MeSH terms: Glycosylation End Products, Advanced/metabolism
  8. Ng ZX, Kuppusamy UR, Iqbal T, Chua KH
    Gene, 2013 Jun 1;521(2):227-33.
    PMID: 23545311 DOI: 10.1016/j.gene.2013.03.062
    Receptor for advanced glycation end-product (RAGE) gene polymorphism 2245G/A is associated with diabetic retinopathy (DR). However, the mechanism on how it affects the disease development is still unclear.
    Matched MeSH terms: Glycosylation End Products, Advanced/metabolism
  9. Einstein JW, Mustafa MR, Nishigaki I, Rajkapoor B, Moh MA
    Methods Find Exp Clin Pharmacol, 2008 Oct;30(8):599-605.
    PMID: 19088944 DOI: 10.1358/mf.2008.30.8.1268401
    The protective effect of methanol extracts of Cassia fistula (flowers, leaves and bark) was examined in vitro in human umbilical vein endothelial cells (HUVEC) against toxicity induced by glycated protein (GFBS) in vitro. The experiments consisted of eight groups of HUVEC with five flasks in each group. Group I was treated with 15% FBS, group II with GFBS (70 microM) alone, and the other six groups were treated with GFBS plus 25 and 50 microg of each of the three types of C. fistula extracts. After 72 h of incubation, cells were collected and tested for lipid peroxidation, antioxidant enzyme activities and glutathione S-transferase (GST). The protective effect of C. fistula extracts against GFBS-induced cytotoxicity was examined in HUVEC by using trypan blue exclusion and MTT assays. Results showed that HUVEC incubated with GFBS alone showed a significant (P < 0.001) elevation of lipid peroxidation accompanied by depletion of superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx) and glutathione reductase (GR), in addition to decreased cytosolic GST. Treatment of HUVEC with C. fistula extracts at a concentration of 25 and 50 microg significantly decreased lipid peroxidation and normalized the activities of the antioxidant enzymes and GST levels in a concentration-dependent manner. Morphological changes of HUVEC were compared with respective controls; in addition, the C. fistula extracts increased the viability of HUVEC damaged by GFBS. A protective effect of C. fistula extracts on HUVEC against GFBS-induced toxicity suggested a potential beneficial effect of the extract in preventing diabetic angiopathies.
    Matched MeSH terms: Glycosylation End Products, Advanced/metabolism
  10. Ali D, Al-Yahya QM, Baskaradoss JK
    Int Dent J, 2023 Oct;73(5):717-723.
    PMID: 37037698 DOI: 10.1016/j.identj.2023.03.005
    OBJECTIVE: The aim of this study was to compare peri-implant clinical and radiographic status and levels of advanced glycation endproducts (AGEs) in peri-implant sulcular fluid (PISF) in waterpipe users and cigarette smokers.

    METHODS: Waterpipe users, cigarette smokers, and never smokers were included. Demographic details were collected using a questionnaire. Characteristics of implants (dimensions, jaw location, depth of placement, insertion torque, and duration in function) were recorded. Peri-implant modified plaque and gingival indices (mPI and mGI), probing depth (PD), and crestal bone loss (CBL) were recorded in all groups. Volume of PISF and levels of AGEs were determined using standard techniques. Sample-size estimation was done on data from a pilot investigation, and correlation between clinicoradiographic and immunoinflammatory parameters was assessed using logistic regression models. Probability values

    Matched MeSH terms: Glycosylation End Products, Advanced
  11. Aftab MF, Afridi SK, Mughal UR, Karim A, Haleem DJ, Kabir N, et al.
    J. Chem. Neuroanat., 2017 04;81:1-9.
    PMID: 28093241 DOI: 10.1016/j.jchemneu.2017.01.001
    Diabetes is associated with neurodegeneration. Glycation ensues in diabetes and glycated proteins cause insulin resistance in brain resulting in amyloid plaques and NFTs. Also glycation enhances gliosis by promoting neuroinflammation. Currently there is no therapy available to target neurodegenration in brain therefore, development of new therapy that offers neuroprotection is critical. The objective of this study was to evaluate mechanistic effect of isatin derivative URM-II-81, an anti-glycation agent for improvement of insulin action in brain and inhibition of neurodegenration. Methylglyoxal induced stress was inhibited by treatment with URM-II-81. Also, Ser473 and Ser9 phosphorylation of Akt and GSK-3β respectively were restored by URM-II-81. Effect of URM-II-81 on axonal integrity was studied by differentiating Neuro2A using retinoic acid. URM-II-81 restored axonal length in MGO treated cells. Its effects were also studied in high fat and low dose streptozotocin induced diabetic mice where it reduced RBG levels and inhibited glycative stress by reducing HbA1c. URM-II-81 treatment also showed inhibition of gliosis in hippocampus. Histological analysis showed reduced NFTs in CA3 hippocampal region and restoration of insulin signaling in hippocampii of diabetic mice. Our findings suggest that URM-II-81 can be developed as a new therapeutic agent for treatment of neurodegenration.
    Matched MeSH terms: Glycosylation End Products, Advanced/antagonists & inhibitors; Glycosylation End Products, Advanced/metabolism
  12. Safi SZ, Qvist R, Kumar S, Batumalaie K, Ismail IS
    Biomed Res Int, 2014;2014:801269.
    PMID: 25105142 DOI: 10.1155/2014/801269
    The growing number of people with diabetes worldwide suggests that diabetic retinopathy (DR) and diabetic macular edema (DME) will continue to be sight threatening factors. The pathogenesis of diabetic retinopathy is a widespread cause of visual impairment in the world and a range of hyperglycemia-linked pathways have been implicated in the initiation and progression of this condition. Despite understanding the polyol pathway flux, activation of protein kinase C (KPC) isoforms, increased hexosamine pathway flux, and increased advanced glycation end-product (AGE) formation, pathogenic mechanisms underlying diabetes induced vision loss are not fully understood. The purpose of this paper is to review molecular mechanisms that regulate cell survival and apoptosis of retinal cells and discuss new and exciting therapeutic targets with comparison to the old and inefficient preventive strategies. This review highlights the recent advancements in understanding hyperglycemia-induced biochemical and molecular alterations, systemic metabolic factors, and aberrant activation of signaling cascades that ultimately lead to activation of a number of transcription factors causing functional and structural damage to retinal cells. It also reviews the established interventions and emerging molecular targets to avert diabetic retinopathy and its associated risk factors.
    Matched MeSH terms: Glycosylation End Products, Advanced/metabolism
  13. Md Isa SH, Najihah I, Nazaimoon WM, Kamarudin NA, Umar NA, Mat NH, et al.
    Diabetes Res Clin Pract, 2006 Apr;72(1):48-52.
    PMID: 16253380 DOI: 10.1016/j.diabres.2005.09.011
    We studied the efficacy of four different treatment regimens (sulphonylurea and metformin+/-acarbose versus glimepiride and rosiglitazone versus glimepiride and bedtime NPH insulin versus multiple actrapid and NPH insulin injections) in poorly controlled type 2 diabetes subjects on hs-CRP, VCAM-1 and AGE at 4, 8 and 12 weeks of treatment. Multiple insulin injections rapidly improved HbA(1c) by 0.6+/-0.9% (p<0.005), 1.2+/-1.3% (p<0.0005) and 1.3+/-1.4% (p<0.0005) at week 4, at week 8 and week 12, respectively. Subjects who continued their existing combination treatment of sulphonylurea, metformin+/-acarbose also showed a significant reduction in HbA(1c) (p<0.05). Although effective in reducing glycemic parameters, there was no reduction in CRP levels in either treatment group. The treatment regimen consisting of rosiglitazone and glimepiride significantly lowered hs-CRP by -2.6 (3.9) mg/L (p<0.05) at week 12 in spite of no improvement in blood glucose. AGE improved in all groups irrespective of type of treatment, glycaemic control and CRP levels. Our data indicate rapid glycaemic control alone does not necessarily result in improvement in markers of inflammation in type 2 diabetes patients.
    Matched MeSH terms: Glycosylation End Products, Advanced/blood*
  14. Zhang X, Liu JJ, Sum CF, Ying YL, Tavintharan S, Ng XW, et al.
    Atherosclerosis, 2015 Sep;242(1):22-8.
    PMID: 26162317 DOI: 10.1016/j.atherosclerosis.2015.06.019
    OBJECTIVE: We previously reported ethnic disparity in adverse outcomes among Asians with type 2 diabetes (T2DM) in Singapore. Central arterial stiffness can aggravate systemic vasculopathy by propagating elevated systolic and pulse pressures forward, thereby accentuating global vascular injury. We aim to study ethnic disparity in central arterial stiffness and its determinants in a multi-ethnic T2DM Asian cohort.
    METHODS: Arterial stiffness was estimated by carotid-femoral pulse wave velocity (PWV) and augmentation index (AI) using applanation tonometry method in Chinese (N = 1045), Malays (N = 458) and Indians (N = 468). Linear regression model was used to evaluate predictors of PWV and AI.
    RESULTS: PWV was higher in Malays (10.1 ± 3.0 m/s) than Chinese (9.7 ± 2.8 m/s) and Indians (9.6 ± 3.1 m/s) (P = 0.018). AI was higher in Indians (28.1 ± 10.8%) than Malays (25.9 ± 10.1%) and Chinese (26.1 ± 10.7%) (P < 0.001). Malays remain associated with higher PWV (β = 0.299, P = 0.048) post-adjustment for age, gender, duration of diabetes, hemoglobin A1c, body mass index (BMI), systolic blood pressure (SBP), diastolic blood pressure (DBP), soluble receptor for advanced glycation end-products, urinary albumin-to-creatinine ratio, and insulin usage, which were all independent predictors of PWV. Indians remain associated with higher AI (β = 2.776, P < 0.001) post-adjustment for age, gender, BMI, SBP, DBP, and height, which were independent predictors of AI. These variables explained 27.7% and 33.4% of the variance in PWV and AI respectively.
    CONCLUSIONS: Malays and Indians with T2DM have higher central arterial stiffness, which may explain their higher risk for adverse outcomes. Modifying traditional major vascular risk factors may partially alleviate their excess cardiovascular risk through modulating arterial stiffness.
    KEYWORDS: Arterial stiffness; Augmentation index; Pulse wave velocity; Type 2 diabetes
    Matched MeSH terms: Glycosylation End Products, Advanced/blood
  15. Zhiping H, Imam MU, Ismail M, Ismail N, Yida Z, Ideris A, et al.
    Food Funct, 2015 May;6(5):1701-11.
    PMID: 25920003 DOI: 10.1039/c5fo00226e
    The aim of this research is to investigate whether edible bird's nest (EBN) attenuates cortical and hippocampal neurodegeneration in ovariectomized rats. Ovariectomized rats were randomly divided into seven experimental groups (n = 6): the ovariectomy (OVX) group had their ovaries surgically removed; the sham group underwent surgical procedure similar to OVX group, but ovaries were left intact; estrogen group had OVX and received estrogen therapy (0.2 mg kg(-1) per day); EBN treatment groups received 6%, 3%, and 1.5% EBN, respectively. Control group was not ovariectomized. After 12 weeks of intervention, biochemical assays were performed for markers of neurodegeneration, and messenger ribonucleic acid (mRNA) levels of oxidative stress-related genes in the hippocampus and frontal cortex of the brain were analysed. Caspase 3 (cysteine-aspartic proteases 3) protein levels in the hippocampus and frontal cortex were also determined using western blotting. The results show that EBNs significantly decreased estrogen deficiency-associated serum elevation of advanced glycation end-products (AGEs), and they changed redox status as evidenced by oxidative damage (malondialdehyde content) and enzymatic antioxidant defense (superoxide dismutase and catalase) markers. Furthermore, genes associated with neurodegeneration and apoptosis were downregulated in the hippocampus and frontal cortex by EBN supplementation. Taken together, the results suggest that EBN has potential for neuroprotection against estrogen deficiency-associated senescence, at least in part via modification of the redox system and attenuation of AGEs.
    Matched MeSH terms: Glycosylation End Products, Advanced/metabolism
  16. Goon JA, Aini AH, Musalmah M, Anum MY, Nazaimoon WM, Ngah WZ
    J Phys Act Health, 2009 Jan;6(1):43-54.
    PMID: 19211957
    BACKGROUND: The biochemical mechanisms involving oxidative stress to explain the relationship between exercise and healthy aging are still unclear.

    METHODS: Tai Chi participants and matched sedentary volunteers age 45 and above were enrolled. Glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase (CAT) activities; levels of DNA damage using the comet assay; and malondialdehyde (MDA) and advanced glycation end products (AGE) were determined at 0, 6, and 12 months.

    RESULTS: Tai Chi subjects had decreased normal and increased mildly damaged DNA with elevated GPx activity after 6 months (n=25). Plasma MDA and AGE concentrations decreased significantly after 12 months (n=15) accompanied by increased SOD activity. This may be attributed to the hormesis effect, whereby mild induction of oxidative stress at the first 6 months of exercise resulted in stimulation of antioxidant defenses. These parameters were unchanged in the sedentary subjects in the first 6 months (n=27) except for elevated SOD activity. After 12 months, the sedentary subjects (n=17) had decreased normal DNA and increased severely damaged DNA with unaltered MDA and AGE levels while SOD and GPx activities were significantly elevated.

    CONCLUSION: Regular Tai Chi exercise stimulated endogenous antioxidant enzymes and reduced oxidative damage markers.

    Matched MeSH terms: Glycosylation End Products, Advanced/blood
  17. Shi B, Guo X, Liu H, Jiang K, Liu L, Yan N, et al.
    Food Chem, 2024 Apr 16;438:137994.
    PMID: 37984001 DOI: 10.1016/j.foodchem.2023.137994
    Foods rich in carbohydrates or fats undergo the Maillard reaction during frying, which promotes the color, flavor and sensory characteristics formation. In the meanwhile, Maillard reaction intermediates and advanced glycation end products (AGEs) have a negative impact on food sensory quality and gut homeostasis. This negative effect can be influenced by food composition and other processing factors. Whole grain products are rich in polyphenols, which can capture carbonyl compounds in Maillard reaction, and reduce the production of AGEs during frying. This review summarizes the Maillard reaction production intermediates and AGEs formation mechanism in fried food and analyzes the factors affecting the sensory formation of food. In the meanwhile, the effects of Maillard reaction intermediates and AGEs on gut homeostasis were summarized. Overall, the innovative processing methods about the Maillard reaction are summarized to optimize the sensory properties of fried foods while minimizing the formation of AGEs.
    Matched MeSH terms: Glycosylation End Products, Advanced*
  18. Nazratun N, Mahmood AA, Kuppusamy UR, Ahmad TS, Tan SY
    Vasc Med, 2006 Nov;11(4):245-50.
    PMID: 17390548
    The excess accumulation of advanced glycation end products (AGEs) contributes to the chronic complications of type 2 diabetes mellitus (DM) and renal failure. Biopsy specimens (n = 184) of arterial (n = 92) and venous (n = 92) tissues were obtained (radial artery and cephalic vein) from end-stage renal disease (ESRD) patients with or without DM and normal healthy subjects (n = 12) requiring surgery (trauma patients). Immunohistochemical assessment of the blood vessels revealed the presence of pentosidine (AGE marker) in both veins and arteries in 72% of the ESRD patients. The percentage of arteries and veins that showed positive pentosidine staining in ESRD patients with type 2 DM alone was 100% and 92% respectively, in the non-diabetic ESRD patients it was < 70% (for arteries and veins), and in the ESRD patients with hypertension as an additional co-morbidity to type 2 DM it was 70% and 82%, respectively. The veins of ESRD patients with DM showed a strong (+++) positive staining and very strong (++++) positive staining was observed in the patients with DM and hypertension. Only mild (+) or moderate (++) pentosidine staining intensity was observed in the arteries of ESRD patients without or with comorbidities, respectively. The accumulation of AGE in the vein rather than the artery may be a better reflection of the extent of complications of ESRD.
    Matched MeSH terms: Glycosylation End Products, Advanced/metabolism*
  19. Kuppusamy UR, Indran M, Ahmad T, Wong SW, Tan SY, Mahmood AA
    Clin Chim Acta, 2005 Jan;351(1-2):197-201.
    PMID: 15563890 DOI: 10.1016/j.cccn.2004.09.014
    BACKGROUND: Comparisons of oxidative indices and total antioxidant status between end-stage renal disease (ESRD) patients with or without diabetes is scant, especially in the Asian population.
    METHOD: The assays were carried out according to known established protocols.
    RESULT: The present study showed that ESRD patients with or without non-insulin-dependent diabetes mellitus (NIDDM) did not have any significant differences in antioxidant enzyme activities, advanced glycated end products (AGE), advanced oxidized protein products (AOPP) and ferric reducing ability of plasma (FRAP), indicating that hyperglycemia does not exacerbate oxidative damage in ESRD. The regulation of catalase and glutathione peroxidase is also altered in ESRD. Elevated FRAP was observed in both ESRD groups (with and without NIDDM). The dialysis process did not alter the antioxidant enzyme activities but decreased AGEs and FRAP and increased AOPP levels.
    CONCLUSION: Oxidative stress is present in ESRD but this is not significantly exacerbated by hyperglycemia. The contribution of components in the pathology of renal failure towards oxidative stress exceeds that of hyperglycemia.
    Matched MeSH terms: Glycosylation End Products, Advanced/blood
  20. Chandramathi S, Suresh K, Anita ZB, Kuppusamy UR
    J Cancer Res Clin Oncol, 2009 Feb;135(2):319-23.
    PMID: 18758816 DOI: 10.1007/s00432-008-0462-7
    PURPOSE: This study aimed to use non-invasive methods to assess and compare the levels of oxidative indices and non-enzymatic antioxidants in breast and colorectal cancer (CRC) patients. Various studies have reported on lipid peroxidation, hydrogen peroxide (H(2)O(2)) and ferric-reducing antioxidant power (FRAP) levels in the serum of cancer patients but this is the first report that highlights the significance of urinary-advanced oxidative protein product (AOPP) in cancer patients.
    METHODS: The levels of advanced oxidative protein product (AOPP), hydrogen peroxide (H(2)O(2)), malondialdehyde (MDA) which is a marker for lipid peroxidation and ferric-reducing antioxidant power (FRAP) were measured in urine samples of breast (n = 101) and colorectal cancer (n = 49) patients attending the Oncology Clinic, University Malaya Medical Centre, Kuala Lumpur and were compared with 95 age-matched healthy individuals.
    RESULTS: AOPP, H(2)O(2) and MDA levels in the urine were significantly higher in the CRC patients compared to the control subjects and breast cancer patients. In breast cancer patients, only AOPP level was elevated. FRAP level did not differ between breast and colorectal cancer patients but the levels were significantly lower compared to control subjects.
    CONCLUSION: Urinary oxidative indices such as AOPP, H(2)O(2), and MDA as well as FRAP could serve as useful non-invasive oxidative stress markers in colorectal cancer but only AOPP serves as a useful urinary oxidative biomarker in breast cancer.
    Study site: Oncology clinic, University Malaya Medical Centre (UMMC), Kuala Lumpur, Malaysia
    Matched MeSH terms: Glycosylation End Products, Advanced/urine*
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