Hydroxyl Radical Mediates Nϵ-(Carboxymethyl)lysine Formation from Amadori Product

Nagai, Ryoji; Ikeda, Kazuyoshi; Higashi, Takayuki; Sano, Hiroyuki; Jinnouchi, Yoshiteru; Araki, Toshimitsu; Horiuchi, Seikoh

doi:10.1006/bbrc.1997.6608

Cited by 169 publications

(117 citation statements)

References 29 publications

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“…Our findings in a previous report suggested that the accumulation of advanced glycation end products (AGEs) in the thoracic aorta from 12-week-old SHRSP was significantly higher than that in age-matched normotensive WKY (20). Several studies have suggested that AGE proteins induce oxidative stress (21,22), and that hydrogen peroxide may be a candidate for reactive oxygen species that contribute to the oxidative damage of smooth muscle cells (23). In addition, findings in a cell culture study we conducted suggested that AGEs dose-dependently increased the 8-OHdG in a bathing solution of cultured smooth muscle cells from SHRSP (submitted).…”

Section: Discussionmentioning

confidence: 47%

Assessment of in vivo Oxidative Stress in Hypertensive Rats and Hypertensive Subjects in Tanzania, Africa.

et al. 2000

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Oxidative stress has been reported to be involved in not only cardiovascular diseases but in hypertension, which is a major risk for cardiovascular diseases. Urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG) has been recognized as a sensitive biomarker of oxidative DNA damage and also of oxidative stress. In the present study, we assessed the oxidative stress in human subjects with hypertension and in hypertensive rats. In stroke-prone spontaneously hypertensive rats at the age of 14 weeks, the excretion of urinary 8-

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Section: Discussionmentioning

confidence: 47%

Assessment of in vivo Oxidative Stress in Hypertensive Rats and Hypertensive Subjects in Tanzania, Africa.

et al. 2000

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“…The first is derived from oxidative cleavage of Amadori adducts (53)(54)(55), the second is derived from Schiff bases (17), and the third is derived from glyoxal generated through autoxidation of glucose (20). In the present study, CML generated 2.5 and 64.0% of modified lysine residues in GA-BSA and GO-BSA, respectively.…”

Section: Discussionmentioning

confidence: 54%

Glycolaldehyde, a reactive intermediate for advanced glycation end products, plays an important role in the generation of an active ligand for the macrophage scavenger receptor.

Nagai

Matsumoto²,

Xia³

et al. 2000

Diabetes

170

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. The negative charge of these ligands increased to a similar extent. However, GA-BSA, but not MG-BSA or GO-BSA, underwent receptor-mediated endocytosis by the macrophage-derived cell line RAW 264.7, which was effectively inhibited by glucose-derived AGE-BSA, acetylated LDL, and oxidized LDL, which are wellknown ligands for the macrophage type I and type II class A scavenger receptors (MSR-A). The endocytic uptake of GA-BSA by mouse peritoneal macrophages was also significant, but that by peritoneal macrophages from MSR-A-deficient mice was markedly reduced. Our results suggest that GA serves as an important intermediate for the generation of AGE structure(s) responsible for recognition by MSR-A.

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“…The H 2 O 2 reacts with Fe 2+ through Fenton reactions to provide a hydroxyl group. Finally hydroxyl group cleavages a C-C bound in Amadori product to make CML as an AGE adduct [76]. From this brief explanation, it seems that phenolic compounds with their antioxidant properties are capable to suppress AGE formation by trapping free radicals.…”

Section: Free Radical Scavengingmentioning

confidence: 99%

The Mechanisms of Inhibition of Advanced Glycation End Products Formation through Polyphenols in Hyperglycemic Condition

et al. 2015

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Glycation, the non-enzymatic binding of glucose to free amino groups of an amino acid, yields irreversible heterogeneous compounds known as advanced glycation end products. Those products play a significant role in diabetic complications. In the present article we briefly discuss the contribution of advanced glycation end products to the pathogenesis of diabetic complications, such as atherosclerosis, diabetic retinopathy, nephropathy, neuropathy, and wound healing. Then we mention the various mechanisms by which polyphenols inhibit the formation of advanced glycation end products. Finally, recent supporting documents are presented to clarify the inhibitory effects of polyphenols on the formation of advanced glycation end products. Phytochemicals apply several antiglycation mechanisms, including glucose metabolism, amelioration of oxidative stress, scavenging of dicarbonyl species, and up/down-regulation of gene expression. To utilize polyphenols in order to remedy diabetic complications, we must explore, examine and clarify the action mechanisms of the components of polyphenols.

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Hydroxyl Radical Mediates Nϵ-(Carboxymethyl)lysine Formation from Amadori Product

Cited by 169 publications

References 29 publications

Assessment of in vivo Oxidative Stress in Hypertensive Rats and Hypertensive Subjects in Tanzania, Africa.

Assessment of in vivo Oxidative Stress in Hypertensive Rats and Hypertensive Subjects in Tanzania, Africa.

Glycolaldehyde, a reactive intermediate for advanced glycation end products, plays an important role in the generation of an active ligand for the macrophage scavenger receptor.

The Mechanisms of Inhibition of Advanced Glycation End Products Formation through Polyphenols in Hyperglycemic Condition

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