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Glycation and Oxidative Stress Increase Autoantibodies in the Elderly.
Khan, MWA, Al Otaibi, A, Sherwani, S, Khan, WA, Alshammari, EM, Al-Zahrani, SA, Saleem, M, Khan, SN, Alouffi, S
Molecules (Basel, Switzerland). 2020;(16)
Abstract
Aging causes gradual changes in free radicals, antioxidants, and immune-imbalance in the elderly. This study aims to understand links among aging, gluco-oxidative stress, and autoantibodies in asymptomatic individuals. In vitro glycation of human serum albumin (Gly-HSA) induces appreciable biochemical changes. Significant inhibition of advanced glycation end products (AGEs) formation was achieved using garlic extract (53.75%) and epigallocatechin-3-gallate from green tea (72.5%). Increased amounts of serum carbonyl content (2.42 ± 0.5) and pentosidine (0.0321 ± 0.0029) were detected in IV-S (S represent smokers) vs. IV group individuals. Direct binding ELISA results exhibited significantly high autoantibodies against Gly-HSA in group IV-S (0.55 ± 0.054; p < 0.001) and III-S (0.40 ± 0.044; p < 0.01) individuals as compared to the age matched subjects who were non-smokers (group IV and III). Moreover, high average percent inhibition (51.3 ± 4.1%) was obtained against Gly-HSA in IV-S group individuals. Apparent association constant was found to be high for serum immunoglobulin-G (IgG) from group IV-S (1.18 × 10-6 M) vs. serum IgG from IV group (3.32 × 10-7 M). Aging induced gluco-oxidative stress and AGEs formation may generate neo-epitopes on blood-proteins, contributing to production of autoantibodies in the elderly, especially smokers. Use of anti-glycation natural products may reduce age-related pathophysiological changes.
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Do advanced glycation end-products play a role in malaria susceptibility?
Traoré, K, Arama, C, Médebielle, M, Doumbo, O, Picot, S
Parasite (Paris, France). 2016;:15
Abstract
There are growing data supporting the differences in susceptibility to malaria described between sympatric populations with different lifestyles. Evidence has also been growing for some time that nutritional status and the host's metabolism are part of the complex mechanisms underlying these differences. The role of dietary advanced glycation end-products (AGEs) in the modulation of immune responses (innate and adaptive responses) and chronic oxidative stress has been established. But less is known about AGE implication in naturally acquired immunity and susceptibility to malaria. Since inflammatory immune responses and oxidative events have been demonstrated as the hallmark of malaria infection, it seems crucial to investigate the role of AGE in susceptibility or resistance to malaria. This review provides new insight into the relationship between nutrition, metabolic disorders, and infections, and how this may influence the mechanisms of susceptibility or resistance to malaria in endemic areas.
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High concentrations of AGE-LDL and oxidized LDL in circulating immune complexes are associated with progression of retinopathy in type 1 diabetes.
Lopes-Virella, MF, Baker, NL, Hunt, KJ, Lyons, TJ, Jenkins, AJ, Virella, G, ,
Diabetes care. 2012;(6):1333-40
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Abstract
OBJECTIVE To determine whether immunocomplexes (ICs) containing advanced glycation end product (AGE)-LDL (AGE-LDL) and oxidized LDL (oxLDL) contribute to the development of retinopathy over a 16-year period in subjects with type 1 diabetes. RESEARCH DESIGN AND METHODS Levels of AGE-LDL and oxLDL in ICs were measured in 517 patients of the Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications (DCCT/EDIC) cohort. Retinopathy was assessed by stereoscopic fundus photography. Cox proportional hazards models were used to assess the effect of AGE-LDL-ICs and oxLDL-ICs on retinopathy progression. RESULTS In unadjusted models, higher baseline levels of AGE-LDL-ICs and oxLDL-ICs significantly predicted progression of diabetic retinopathy outcomes. After adjustment by study-design variables (treatment group, retinopathy cohort, duration of type 1 diabetes, and baseline albumin excretion rate [AER], hemoglobin A(1c) (HbA(1c)), and Early Treatment Diabetic Retinopathy Study [ETDRS] score), one SD increase in IC levels was associated with 47% (hazard ratio [HR] 1.47 [95% CI 1.19-1.81]; AGE-LDL-IC) and 45% (1.45 [1.17-1.80]; oxLDL-IC) increased risk of developing proliferative diabetic retinopathy (PDR) and 37% (1.37 [1.12-1.66]; to both ICs) increased risk of progressing to severe nonproliferative retinopathy. Analyses were stratified by retinopathy cohort because results differed between primary and secondary cohorts. For AGE-LDL-ICs, HR for progression to PDR was 2.38 (95% CI 1.30-4.34) in the primary cohort and attenuated in the secondary cohort (1.29 [1.03-1.62]). Similar results were observed for oxLDL-ICs. CONCLUSIONS Increased levels of AGE-LDL and oxLDL in ICs are associated with increased risk for progression to advanced retinopathy in patients with type 1 diabetes, indicating that the antibody response to modified LDL plays a significant role in retinopathy progression.
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Ciprofloxacin inhibits advanced glycation end products-induced adhesion molecule expression on human monocytes.
Mori, S, Takahashi, HK, Liu, K, Wake, H, Zhang, J, Liu, R, Yoshino, T, Nishibori, M
British journal of pharmacology. 2010;(1):229-40
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Abstract
BACKGROUND AND PURPOSE Advanced glycation end products (AGEs) subtypes, proteins or lipids that become glycated after exposure to sugars, can induce complications in diabetes. Among the various AGE subtypes, glyceraldehyde-derived AGE (AGE-2) and glycolaldehyde-derived AGE (AGE-3) are involved in inflammation in diabetic patients; monocytes are activated by these AGEs. Ciprofloxacin (CIP), a fluorinated 4-quinolone, is often used clinically to treat infections associated with diabetis due to its antibacterial properties. It also modulates immune responses in human peripheral blood mononuclear cells (PBMC) therefore we investigated the involvement of AGEs in these effects. EXPERIMENTAL APPROACH Expression of intercellular adhesion molecule (ICAM)-1, B7.1, B7.2 and CD40 was examined by flow cytometry. The production of tumour necrosis factor (TNF)-alpha, interferon (IFN)-gamma, prostaglandin E(2) (PGE(2)) and cAMP were determined by enzyme-linked immunosorbent assay. Cyclooxygenase (COX)-2 expression was determined by Western blot analysis. Lymphocyte proliferation was determined by [(3)H]-thymidine uptake. KEY RESULTS CIP induced PGE(2) production in monocytes, irrespective of the presence of AGE-2 and AGE-3, by enhancing COX-2 expression; this led to an elevation of intracellular cAMP in monocytes. Non-selective and selective COX-2 inhibitors, indomethacin and NS398, inhibited CIP-induced PGE(2) and cAMP production. In addition, CIP inhibited AGE-2- and AGE-3-induced expressions of ICAM-1, B7.1, B7.2 and CD40 in monocytes, the production of TNF-alpha and IFN-gamma and lymphocyte proliferation in PBMC. Indomethacin, NS398 and a protein kinase A inhibitor, H89, inhibited the actions of CIP. CONCLUSIONS AND IMPLICATIONS CIP exerts immunomodulatory activity via PGE(2), implying therapeutic potential of CIP for the treatment of AGE-2- and AGE-3-induced inflammatory responses.
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[Advanced glycation and lipoxidation end products--amplifiers of inflammation: the role of food].
Gil, A, Bengmark, S
Nutricion hospitalaria. 2007;(6):625-40
Abstract
Chronic diseases (CD) represent the main cause of mortality in developed countries. The increase in the prevalence of of CD is associated with changes in lifestyle habits, including those related to the consumption of processed foodstuffs. In these foods advanced glycation end products (AGE) and advanced lipoperoxydation products (ALE) are formed as a consequence of the reactivity of proteins, carbohydrates, lipid and other components. The aim of the present review is to offer a perspective of how AGE and ALE affect the physiology and development of CD. Continous intake of AGE and ALE contributes to the exccesive accumulation of these products into body tissues, which in turn negatively influence the innate immune system, inflammatory responses, and resistance to diseases. This is achieved by direct interaction of AGE and ALE with specific cell AGE receptors (RAGE) that have a key role as master switches regulating the development of CD. Long-life molecules, namely collagen and myelin, and low-turnover tissues, e.g. connective, bone and neural tissues, are the main targets of AGE and ALE. In these tissues, AGE and ALE lead to the synthesis of insoluble compounds that severely alter cellular functionality. It has been reported associations of AGE and ALE with allergic and autoimmune diseases, Alzheimer disease and other degenerative disorders, catarats, atherosclerosis, cancer, and diabetes mellitus type 2, as well as a number of endocrine, gastrointestinal, skeleton-muscle, and urogenital alterations. Controlling all those pathologies would need further dietary recommendations aiming to limit the intake of processed foods rich in AGE and ALE, as well as to reduce the formation of those products by improving technological processes applicable to foods.