Glycation of aspartate aminotransferase by methylglyoxal, effect of hydroxycitric and uric acid
Language English Country Netherlands Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
- MeSH
- Aspartate Aminotransferases chemistry metabolism MeSH
- Citrates pharmacology MeSH
- Fluorescence MeSH
- Glycosylation drug effects MeSH
- Protein Structure, Quaternary MeSH
- Uric Acid pharmacology MeSH
- Ornithine analogs & derivatives metabolism MeSH
- Glycation End Products, Advanced metabolism MeSH
- Pyrimidines metabolism MeSH
- Pyruvaldehyde pharmacology MeSH
- Cross-Linking Reagents pharmacology MeSH
- Sus scrofa MeSH
- Blotting, Western MeSH
- Animals MeSH
- Check Tag
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- argpyrimidine MeSH Browser
- Aspartate Aminotransferases MeSH
- Citrates MeSH
- hydroxycitric acid MeSH Browser
- Uric Acid MeSH
- Ornithine MeSH
- Glycation End Products, Advanced MeSH
- Pyrimidines MeSH
- Pyruvaldehyde MeSH
- Cross-Linking Reagents MeSH
Glycation is a process closely related to the aging and pathogenesis of diabetic complications. Reactive alpha-dicarbonyl compounds (e.g., methylglyoxal) are formed during middle stage of glycation reaction. Compounds that would inhibit the glycation process have been seeked for years. The objective of this study was to investigate the inhibitory effect of hydroxycitric (0.25-2.5 mM) and uric acid (0.4-1.2 mM) on middle stage of protein glycation in vitro using the model containing aspartate aminotransferase (AST) and 0.5 mM methylglyoxal. Hydroxycitric acid, at all tested concentrations, reduced AST activity decrease and formation of fluorescent AGEs during incubation of the enzyme with methylglyoxal at 37 degrees C. This compound also prevented formation of high-molecular weight protein cross-links and changes in molecular charge of AST caused by glycation. Uric acid showed no positive anti-glycation activity. The results support the hypothesis that hydroxycitric acid has beneficial effects in controlling protein glycation.
See more in PubMed
Arch Biochem Biophys. 1969 Dec;135(1):209-17 PubMed
Food Chem Toxicol. 2004 Sep;42(9):1513-29 PubMed
Invest Ophthalmol Vis Sci. 2003 Dec;44(12):5287-92 PubMed
J Biol Chem. 2001 Apr 20;276(16):13348-55 PubMed
Mol Cell Biochem. 2004 May;260(1-2):171-86 PubMed
Anal Biochem. 1983 Dec;135(2):409-15 PubMed
Arch Biochem Biophys. 2003 Nov 1;419(1):31-40 PubMed
Biochem J. 1988 Nov 15;256(1):205-12 PubMed
Arch Biochem Biophys. 2003 Feb 1;410(1):149-54 PubMed
Toxicol Appl Pharmacol. 1999 Apr 15;156(2):96-105 PubMed
Diabet Med. 2000 Mar;17(3):171-80 PubMed
Lipids. 1974 Feb;9(2):121-8 PubMed
Am J Nephrol. 2004 Jan-Feb;24(1):32-40 PubMed
Physiol Behav. 2006 Jul 30;88(4-5):371-81 PubMed
J Clin Chem Clin Biochem. 1986 Jul;24(7):497-510 PubMed
Nature. 1970 Aug 15;227(5259):680-5 PubMed
Free Radic Biol Med. 1993 Jun;14(6):615-31 PubMed
Lipids. 1974 Feb;9(2):129-34 PubMed
J Pharm Biomed Anal. 2005 Apr 29;37(5):957-62 PubMed
Expert Opin Investig Drugs. 2008 Jul;17(7):983-96 PubMed
Biochem Pharmacol. 2000 Jul 1;60(1):55-65 PubMed
Gen Pharmacol. 1996 Jun;27(4):565-73 PubMed
Biochem J. 1986 May 1;235(3):747-54 PubMed
J Nutr Sci Vitaminol (Tokyo). 1997 Aug;43(4):463-9 PubMed
Arch Biochem Biophys. 2002 Jan 15;397(2):360-9 PubMed
J Biol Chem. 1998 Sep 25;273(39):25272-8 PubMed
Clin Sci (Lond). 1994 Jul;87(1):21-9 PubMed
J Agric Food Chem. 2005 Apr 20;53(8):3167-73 PubMed
J Agric Food Chem. 2002 Jan 2;50(1):10-22 PubMed
Biochem Pharmacol. 1998 May 15;55(10):1667-71 PubMed
Mol Cell Biochem. 2005 Oct;278(1-2):85-92 PubMed
Biochem J. 2000 Nov 15;352 Pt 1:233-40 PubMed
Int J Clin Pharmacol Res. 2005;25(3):133-44 PubMed
Am J Clin Nutr. 1991 Dec;54(6 Suppl):1129S-1134S PubMed
Recent Prog Horm Res. 2001;56:1-21 PubMed
Mol Cell Biochem. 2002 Sep;238(1-2):89-103 PubMed
Diabetes Metab Res Rev. 2004 Sep-Oct;20(5):369-82 PubMed