Keto Acids Pyruvic Acid Tryptophan Transaminase Pyruvates Phenylpyruvic Acids Ketone Oxidoreductases Indoleacetic Acids Caproates 3-Methyl-2-Oxobutanoate Dehydrogenase (Lipoamide) Transaminases Ketoglutaric Acids Lactates Carboxy-Lyases Amino Acids, Branched-Chain Lactic Acid p-Fluorophenylalanine Culture Media Indoles Leucine Isoleucine
reaction products are named advanced glycation end products (AGEs) when the attacking RCS is derived from sugar, and called advanced lipoxidation end products (ALEs) when it derives from lipids. AGEs and ALEs share similar structural and biological properties. For example, both consist of 28.05.2015 Reactive carbonyl species generated by lipid peroxidation are involved in several human diseases and may represent a novel drug target. RCS therefore represent a new biological target for drug disc 71 Curtis TM, Hamilton R, Yong PH et al. Muller glial dysfunction during diabetic retinopathy in rats is linked to accumulation of advanced glycation end-products and advanced lipoxidation end-products. Diabetologia 54(3),690–698 (2011).Crossref, Medline, CAS, Google Scholar
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Advanced lipoxidation end-products, such as MDA- and 4-HNE-protein adducts, can promote monocyte activation and vascular complications via induction of inflammatory pathways and networks . In monocytes, ALEs can lead to cellular dysfunction, adhesion to the endothelium, and transmigration into the subendothelial space, through several monocyte-macrophage inflammatory cytokines and chemokines.
reaction products are named advanced glycation end products (AGEs) when the attacking RCS is derived from sugar, and called advanced lipoxidation end products (ALEs) when it derives from lipids. AGEs and ALEs share similar structural and biological properties. For example, both consist of 28.05.2015 Reactive carbonyl species generated by lipid peroxidation are involved in several human diseases and may represent a novel drug target. RCS therefore represent a new biological target for drug disc 71 Curtis TM, Hamilton R, Yong PH et al. Muller glial dysfunction during diabetic retinopathy in rats is linked to accumulation of advanced glycation end-products and advanced lipoxidation end-products. Diabetologia 54(3),690–698 (2011).Crossref, Medline, CAS, Google Scholar (2000). An advanced glycation end product cross-link breaker can reverse age-related increases in myocardial stiffness. Proceedings of the National Academy of Sciences of the United States of America, 97(6), 2809-2813. Basta, G., Schmidt, A. M., De Caterina, R. (2004). Advanced glycation end products and vascular inflammation implications for aldo-keto reductase family 1, the role of AKR1B3 in regulating advanced glycosylation end products and advanced lipoxidation end products PMID: 21276777; Genetic deficiency of Ar significantly ameliorated development of key endpoints linked with early diabetic nephropathy in vivo.
Advanced lipoxidation end products (ALEs) and advanced glycation end products (AGEs) have a pathogenetic role in the development and progression of
the role of AKR1B3 in regulating advanced glycosylation end products and advanced lipoxidation end products; Genetic deficiency of Ar significantly ameliorated development of key endpoints linked with early diabetic nephropathy in vivo. a Y48F/H110F double mutant of AKR1B3 completely lost PGDS activity and showed only 2.9% of PGFS activity RCs react with proteins to form advanced lipoxidation end products (ALEs; [5,6], which are also known to cause oxidative cell dysfunction. Photosynthesis is the largest biological activity on earth involving anabolic sugar metabolism, and has the potential to generate sugar-derived and lipid-Abbreviations Most of the biological effects of intermediate RCS, mainly α,β‐unsaturated aldehydes, di‐aldehydes, and keto‐aldehydes, are due to their capacity to react with the nucleophilic sites of proteins, forming advanced lipoxidation end‐products (ALEs). Purpose: We studied whether the accumulation of advanced lipoxidation end-products (ALEs) in the diabetic retina is linked to the impairment of lipid aldehyde detoxification mechanisms. Methods: Retinas were collected from nondiabetic and diabetic rats and processed for conventional and quantitative RT-PCR (qRT-PCR), Western blotting, immunohistochemistry, and aldehyde dehydrogenase (ALDH The Amadori products undergo dehydration and rearrangements and develop a cross-link between adjacent proteins, giving rise to protein aggregation or advanced glycation end products (AGEs). A number of studies have shown that glycation induces the formation of the β-sheet structure in β-amyloid protein, α-synuclein, transthyretin (TTR), copper-zinc superoxide dismutase 1 (Cu, Zn-SOD-1), and peroxidation (lipoxidation) reactions in vitro, and we show that it traps reactive intermediates formed during lipid peroxidation. In reactions of arachidonate with the model protein RNase, PM prevented modification of ly-sine residues and formation of the advanced lipoxida-tion end products (ALEs) Ne-(carboxymethyl)lysine, Ne-
kenals, 4-hydroxy–2-alkenals, keto-alkenals, and alkanedial (dia-ldehydes) [3]. The most reactive and commonly studied are mal-ondialdehyde (MDA), acrolein (ACR), 4-hydroxyhexanal (4-HHE) and 4-hydroxynonenal (HNE), which also reflects the fact that these products are produced at higher levels than many other
Most of the biological effects of RCS, mainly alpha,beta-unsaturated aldehydes, di-aldehydes, and keto-aldehydes, are due to their capacity to react with cellular constituents, forming advanced lipoxidation end-products (ALEs). Specific carbonyls, such as alpha-dicarbonyls, may be aldehydic or ketonic (or both) , and are very potent Maillard reaction intermediates, yielding advanced glycation end products (AGEs) as well as advanced lipoxidation end products (ALEs). the role of AKR1B3 in regulating advanced glycosylation end products and advanced lipoxidation end products; Genetic deficiency of Ar significantly ameliorated development of key endpoints linked with early diabetic nephropathy in vivo. a Y48F/H110F double mutant of AKR1B3 completely lost PGDS activity and showed only 2.9% of PGFS activity