AGEs(エージス、エイジス、エイジズ、エージーイー)とは、Advanced Glycation End Productsの略語であり、終末糖化産物、後期糖化生成物などと訳される。タンパク質または脂質が糖へ曝露されることによる糖化反応(メイラード反応)によって作られた生成物の総称であり[1]、身体の様々な老化に関与する物質(より正確に言えば、生体化学反応による生成物)と言える。現在判明しているだけでも、AGEsには数十種類の化合物があり、それぞれが多種多様な化学的性質を有する。AGEsの例としては、Nε-カルボキシメチルリシン(CML)、Nε-カルボキシエチルリシン(CEL)、アルグピリミジンなどが知られている。類似の概念に過酸化脂質に由来する終末過酸化産物(Advanced Lipoxidation End products、ALEs)がある[2]。(ALEsについては脂質過酸化反応も参照の事)
AGEsは、“Advanced Glycation End Product”という英語の頭文字“AGE”に加えて、それが複数形であることを示す“s”を付して名付けられた[3]。Nε-カルボキシメチルリシン(CML)[4]、Nε-カルボキシエチルリシン(CEL)[5]、アルグピリミジン、ペントシジン(英語版)[6]、ピラリン[7]、クロスリン[8]、GA-ピリジン[9]、Nω-カルボキシメチルアルギニン(CMA)[10]、フロイルフラニルイミダゾール(2-(2-furoyl)-4(5)-(2-furanyl)-1H-imidazole)、グルコスパン(英語版)など多数の化合物が特定されている[11]。
Vistoli,G;De Maddis, D;Cipak, A;Zarkovic, N;Carini, M;Aldini, G(Aug 2013).“Advanced glycoxidation and lipoxidation end products (AGEs and ALEs): an overview of their mechanisms of formation.”.Free Radic Res.47(12): Suppl 1:3–27.doi:10.3109/10715762.2013.815348.PMID10946212.
Goldin A, Beckman JA, Schmidt AM, Creager MA(2006).“Advanced glycation end products: sparking the development of diabetic vascular injury”.Circulation114(6): 597–605.doi:10.1161/CIRCULATIONAHA.106.621854.PMID16894049.
Dominiczak MH(2003).“Obesity, glucose intolerance and diabetes and their links to cardiovascular disease. Implications for laboratory medicine”.Clin. Chem. Lab. Med.41(9): 1266–78.doi:10.1515/CCLM.2003.194.PMID14598880.
Gugliucci,A(October 2000).“Glycation as the glucose link to diabetic complications.”.The Journal of the American Osteopathic Association100(10): 621–34.PMID11105451.
Glenn,J.;Stitt,A.(2009).“The role of advanced glycation end products in retinal ageing and disease”.Biochimica et Biophysica Acta1790(10): 1109–1116.doi:10.1016/j.bbagen.2009.04.016.PMID19409449.
Yan,S. F.;D'Agati,V.;Schmidt,A. M.;Ramasamy,R.(2007).“Receptor for Advanced Glycation Endproducts (RAGE): a formidable force in the pathogenesis of the cardiovascular complications of diabetes & aging”.Current molecular medicine7(8): 699–710.doi:10.2174/156652407783220732.PMID18331228.
Pertyńska-Marczewska,M;Głowacka, E;Sobczak, M;Cypryk, K;Wilczyński, J(February 2009).“Glycation endproducts, soluble receptor for advanced glycation endproducts and cytokines in diabetic and non-diabetic pregnancies.”.American journal of reproductive immunology (New York, N.Y.: 1989)61(2): 175–82.doi:10.1111/j.1600-0897.2008.00679.x.PMID19143681.
Srikanth,V;Maczurek, A;Phan, T;Steele, M;Westcott, B;Juskiw, D;Münch, G(May 2011).“Advanced glycation endproducts and their receptor RAGE in Alzheimer's disease.”.Neurobiology of Aging32(5): 763–77.doi:10.1016/j.neurobiolaging.2009.04.016.PMID19464758.
Simm,A;Wagner, J;Gursinsky, T;Nass, N;Friedrich, I;Schinzel, R;Czeslik, E;Silber, REet al.(July 2007).“Advanced glycation endproducts: a biomarker for age as an outcome predictor after cardiac surgery?”.Experimental Gerontology42(7): 668–75.doi:10.1016/j.exger.2007.03.006.PMID17482402.
Zimmerman GA, Meistrell M 3rd, Bloom O, et al.(1995-04-25).“Neurotoxicity of advanced glycation endproducts during focal stroke and neuroprotective effects of aminoguanidine.”.Proc Natl Acad Sci USA.92(9): 3744-8.PMID7731977.
Shaikh S, Nicholson LF(2008-07).“Advanced glycation end products induce in vitro cross-linking of alpha-synuclein and accelerate the process of intracellular inclusion body formation.”.J Neurosci Res.86(9): 2071-82.doi:10.1002/jnr.21644.PMID18335520.
Gul A, Rahman MA, Hasnain SN(2009-06).“Role of fructose concentration on cataractogenesis in senile diabetic and non-diabetic patients.”.Graefes Arch Clin Exp Ophthalmol.247(6): 809-14.doi:10.1007/s00417-008-1027-9.PMID19198870.
Haus,JM;Carrithers, JA;Trappe, SW;Trappe, TA(December 2007).“Collagen, cross-linking, and advanced glycation end products in aging human skeletal muscle.”.Journal of applied physiology (Bethesda, Md.: 1985)103(6): 2068–76.doi:10.1152/japplphysiol.00670.2007.PMID17901242.
Wells-Knecht KJ, Zyzak DV, Litchfield JE, Thorpe SR, Baynes JW(1995).“Mechanism of autoxidative glycosylation: identification of glyoxal and arabinose as intermediates in the autoxidative modification of proteins by glucose”.Biochemistry34(11): 3702–9.doi:10.1021/bi00011a027.PMID7893666.
Gugliucci A, Mehlhaff K, Kinugasa E(2007).“Paraoxonase-1 concentrations in end-stage renal disease patients increase after hemodialysis: correlation with low molecular AGE adduct clearance”.Clin. Chim. Acta377(1–2): 213–20.doi:10.1016/j.cca.2006.09.028.PMID17118352.
Svistounov D, Smedsrød B(2004).“Hepatic clearance of advanced glycation end products (AGEs)—myth or truth?”.J. Hepatol.41(6): 1038–40.doi:10.1016/j.jhep.2004.10.004.PMID15582139.
Hira Zafar,(26 June 2012).“Inhibition of protein glycation and advanced glycation end products by ascorbic acid”.African Journal of Biotechnology11(51).doi:10.5897/AJB11.4172.
Guiotto A, Calderan A, Ruzza P, Borin G(2005).“Carnosine and carnosine-related antioxidants: a review”.Current Medicinal Chemistry12(20): 2293–2315.doi:10.2174/0929867054864796.PMID16181134.
“N-Acetyl Cysteine Attenuated the Deleterious Effects of Advanced Glycation End-Products on the Kidney of Non-Diabetic Rats”.Cellular Physiology and Biochemistry40(3-4).(2016).doi:10.1159/000452574.
Upadhyay A, Tuenter E, Ahmad R, et al.(2014-08).“Kavalactones, a novel class of protein glycation and lipid peroxidation inhibitors.”.Planta Med.80(12): 1001-8.doi:10.1055/s-0034-1382949.PMID25098935.
Monnier, V. M., Mustata, G. T., Biemel, K. L., Reihl, O., Lederer, M. O., Zhenyu, D.(2005).“Cross-linking of the extracellular matrix by the maillard reaction in aging and diabetes: An update on "a puzzle nearing resolution"”.Annals of the New York Academy of Sciences1043: 533–544.doi:10.1196/annals.1333.061.PMID16037276.