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Mol Cell Biochem. 2007 Apr;298(1-2):195-8. Epub 2006 Nov 29.

Premature aging in uremia.

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1
Department of Medicine, Albert Einstein College of Medicine, 1300 Morris Park Ave., Bronx, NY 10469, USA. burt1071@aol.com

Abstract

Guanidinosuccinic acid is an aberrant metabolite isolated 40 years ago in the blood and urine of uremic subjects and a suspect in the toxicity associated with renal failure. It plays a minor role in the bleeding diathesis of uremia, contributes to the methyl group deficiency of dialysis patients, and is a factor in the premature atherosclerosis of end stage renal disease through the induction of hyperhomocysteinemia. As a major player, however, in the diversity and severity of uremic symptoms, it is a disappointment. Recently its source has been identified. It results from the superoxidation of argininosuccinic acid, which leads, also, to the production of gamma glutamic semialdehyde, an advanced glycation end product (AGE), which normally results from from the Maillard reaction, the non-enzymatic browning of protein. AGEs stimulate cross-linkages in protein that lead ultimately to loss of function, phagocytosis, and removal, and are important elements in the premature aging characteristic of renal disease, and diabetes.

PMID:
17136440
DOI:
10.1007/s11010-006-9351-z
[Indexed for MEDLINE]
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