Increased Aggregation of Human Platelets Produced by Advanced Glycation End Productsin Vitro

Advanced glyco-oxidation end products (AGEs) generate oxygen free radicals that potentiate the development of atherosclerosis. Thus, AGEs may potentiate the aggregation of human platelets through oxidative stress. AGE-bovine serum albumin (BSA) and AGE-poly-L-lysine were evaluated for aggregation of...

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Published in:Biochemical and biophysical research communications 1998-07, Vol.248 (2), p.285-292
Main Authors: Hangaishi, Misako, Taguchi, Junichi, Miyata, Toshio, Ikari, Yuji, Togo, Masako, Hashimoto, Yoshiaki, Watanabe, Tsuyoshi, Kimura, Satoshi, Kurokawa, Kiyoshi, Ohno, Minoru
Format: Article
Language:English
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Summary:Advanced glyco-oxidation end products (AGEs) generate oxygen free radicals that potentiate the development of atherosclerosis. Thus, AGEs may potentiate the aggregation of human platelets through oxidative stress. AGE-bovine serum albumin (BSA) and AGE-poly-L-lysine were evaluated for aggregation of human platelets. Superoxide in platelet-rich plasma (PRP) was measured using lucigenin-derived chemiluminescence. The platelet aggregation induced by ADP or U46619 was potentiated by preincubation with AGE-BSA, by 40% and by 59%, P < .05, respectively, vs BSA. Aggregation was increased by AGEs in a dose-dependent manner. The production of superoxide was significantly greater in PRP incubated with AGE-BSA vs BSA. The other Maillard reaction products, such as Amadori-, pentosidine-, and carboxymethyl lysine (CML)-BSA had no effect. Superoxide dismutase or indomethacin abolished the enhancing effect of AGEs on the platelet aggregation. AGEs potentiate platelet aggregation possibly with superoxide anions and prostanoids. AGE-induced potentiation of platelet aggregation may be involved in the development of atherosclerosis.
ISSN:0006-291X
1090-2104
DOI:10.1006/bbrc.1998.8945