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Open AccessJournal ArticleDOI

Imidazolium crosslinks derived from reaction of lysine with glyoxal and methylglyoxal are increased in serum proteins of uremic patients: evidence for increased oxidative stress in uremia.

TLDR
Levels of GOLD and MOLD are significantly elevated in sera of non‐diabetic uremic patients, compared to age‐matched controls, and represent a major class of non-enzymatic, Maillard reaction crosslinks in plasma proteins, implicating oxidative stress and resultant advanced glycation and lipoxidation reactions in tissue damage in uremia.
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Advanced glycation end products and vascular inflammation: implications for accelerated atherosclerosis in diabetes.

TL;DR: A better understanding of the biochemical mechanisms by which AGEs contribute to such processes in the vessel wall could be relevant to devise preventive and therapeutic strategies for diabetic atherosclerosis.
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Aldehyde sources, metabolism, molecular toxicity mechanisms, and possible effects on human health.

TL;DR: The human health risks from clinical and animal research studies are reviewed, including aldehydes as haptens in allergenic hypersensitivity diseases, respiratory allergies, and idiosyncratic drug toxicity; the potential carcinogenic risks of the carbonyl body burden.
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Alterations in nonenzymatic biochemistry in uremia: Origin and significance of “carbonyl stress” in long-term uremic complications

TL;DR: Uremia may be described as a state of carbonyl overload or "carbonyl stress" resulting from either increased oxidation of carbohydrates and lipids (oxidative stress) or inadequate detoxification or inactivation of reactive carbonyL compounds derived from both carbohydrates andlipids by oxidative and nonoxidatives.
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Novel inhibitors of advanced glycation endproducts

TL;DR: A new class of compounds are developed as potent inhibitors of glycation and AGE formation, including aryl (and heterocyclic) ureido, and ary l carboxamido phenoxy isobutyric acids and related molecules, which were found by in vitro assay methods to be potent inhibitors.
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Advanced glycation end products: A nephrologist's perspective

TL;DR: There is an exciting possibility that the complications of diabetes, uremia, and aging may be prevented with these novel agents.
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Journal Article

Protein Measurement with the Folin Phenol Reagent

TL;DR: Procedures are described for measuring protein in solution or after precipitation with acids or other agents, and for the determination of as little as 0.2 gamma of protein.
Journal ArticleDOI

The advanced glycation end product, Nepsilon-(carboxymethyl)lysine, is a product of both lipid peroxidation and glycoxidation reactions.

TL;DR: The results suggest that lipid peroxidation, as well as glycoxidation, may be an important source of CML in tissue proteins in vivo and that CML may be a general marker of oxidative stress and long term damage to protein in aging, atherosclerosis, and diabetes.
Journal ArticleDOI

N-epsilon-(carboxyethyl)lysine, a product of the chemical modification of proteins by methylglyoxal, increases with age in human lens proteins.

TL;DR: Levels of CML and CEL are proposed to provide an index of glyoxal and methylglyoxal concentrations in tissues, alterations in glutathione homoeostasis and dicarbonyl metabolism in disease, and sources of advanced glycation end-products in tissue proteins in aging and disease.
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Glycation and diabetic complications

TL;DR: A review of the mechanisms behind advanced glycation end products (AGEs) play a central role in the pathogenesis of diabetic complications and their effects on diabetic pathology concludes with a summary of AGE inhibition.
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