Inhibition of human muscle-specific enolase by methylglyoxal and irreversible formation of advanced glycation end products

@article{Pietkiewicz2009InhibitionOH,
  title={Inhibition of human muscle-specific enolase by methylglyoxal and irreversible formation of advanced glycation end products},
  author={Jadwiga Pietkiewicz and Andrzej Gamian and Magdalena Maria Staniszewska and Regina Danielewicz},
  journal={Journal of Enzyme Inhibition and Medicinal Chemistry},
  year={2009},
  volume={24},
  pages={356 - 364}
}
Methylglyoxal (MG) was studied as an inhibitor and effective glycating factor of human muscle-specific enolase. The inhibition was carried out by the use of a preincubation procedure in the absence of substrate. Experiments were performed in anionic and cationic buffers and showed that inhibition of enolase by methylglyoxal and formation of enolase-derived glycation products arose more effectively in slight alkaline conditions and in the presence of inorganic phosphate. Incubation of 15… 
10 Citations
Glycation of the Muscle-Specific Enolase by Reactive Carbonyls: Effect of Temperature and the Protection Role of Carnosine, Pirydoxamine and Phosphatidylserine
TLDR
It is demonstrated for the first time that phosphatidylserine may significantly protect enolase against decrease of catalytic activity in spite of AGE production and pirydoxamine and natural dipeptide carnosine counteracted AGE formation and protected enol enzyme against the total loss of catalytical activity.
In Vitro Study of Glycation of Pyruvate Kinase and Its Effect on Activity and Proteolytic Resistance In Absence And Presence Of Aminoguanidine
Protein glycation participates in structural changes that impair protein functionality and this process is related to pathogenesis of diabetes and several diseases. This in vitro study was aimed to
Glycoxidation of biological macromolecules: a critical approach to halt the menace of glycation.
TLDR
The prevention of glycation reaction using therapeutic drugs such as metformin, pyridoxamine and aminoguanidine are discussed with special emphasis on the novel concept of the bioconjugation of these drugs like, AG with gold nanoparticles (GNPs).
The Genotoxic and Pro-Apoptotic Activities of Advanced Glycation End-Products (MAGE) Measured with Micronuclei Assay Are Inhibited by Their Low Molecular Mass Counterparts
TLDR
By measuring of micronuclei in human lymphocytes in vitro that the studied HMW–MAGEs expressed the genotoxicity, it is observed that human melanoma and all other studied cells, such as bronchial epithelial cells, lung cancer cells and colorectal cancer cells, are susceptible to thegenotoxic effects of HMW-Mages.
Fluoride Exposure Induces Inhibition of Sodium-and Potassium-Activated Adenosine Triphosphatase (Na+, K+-ATPase) Enzyme Activity: Molecular Mechanisms and Implications for Public Health
  • Declan T Waugh
  • Medicine
    International journal of environmental research and public health
  • 2019
TLDR
The findings of this study suggest that there are windows of susceptibility over the life course where chronic F exposure in pregnancy and early infancy may impair Na+, K+-ATPase activity with both short- and long-term implications for disease and inequalities in health.
Anticancer Agents That Counteract Tumor Glycolysis
TLDR
There is growing evidence to support many glycolytic enzymes and transporters as suitable candidate targets for cancer therapy, and some of the most relevant antigly colytic agents that have been investigated thus far for the treatment of cancer are reviewed.
The Contribution of Fluoride to the Pathogenesis of Eye Diseases: Molecular Mechanisms and Implications for Public Health
  • Declan T Waugh
  • Medicine
    International journal of environmental research and public health
  • 2019
TLDR
Based on the evidence presented, it can be concluded that F exposure may be added to the list of identifiable risk factors associated with pathogenesis of degenerative eye diseases and reducing F intake may lead to an overall reduction in the modifiable risk factors.

References

SHOWING 1-10 OF 59 REFERENCES
Effect of phosphate on the kinetics and specificity of glycation of protein.
TLDR
Overall, these studies establish that buffering ions or ligands can exert significant effects on the kinetics and specificity of glycation of proteins.
The formation of methylglyoxal from triose phosphates. Investigation using a specific assay for methylglyoxal.
TLDR
The reactivity of glycerone phosphate and glyceraldehyde 3-phosphate towards the non-enzymatic formation of methylglyoxal under physiological conditions suggests that methylglyxal formation is unavoidable from the Embden-Meyerhof pathway.
Identification of N epsilon-carboxymethyllysine as a degradation product of fructoselysine in glycated protein.
TLDR
The browning of fFL incubation mixtures proceeded to a greater extent under a nitrogen versus an air atmosphere, suggesting that oxidative degradation of Amadori adducts to form CML may limit the browning reactions of glycated proteins.
Chromatographic quantification of argpyrimidine, a methylglyoxal-derived product in tissue proteins: comparison with pentosidine.
TLDR
Results from this study confirm that MG-mediated arginine modifications occur in vivo and provide a method for assessing protein-arginine modification by MG in aging and diabetes.
Formation of glyoxal, methylglyoxal and 3-deoxyglucosone in the glycation of proteins by glucose.
TLDR
Alpha-Oxoaldehydes were formed in early glycation from the degradation of glucose and Schiff's base adduct, which suggests that short periods of hyperglycaemia, as occur in impaired glucose tolerance, may be sufficient to increase the concentrations of alpha-oxoaldeHydes in vivo.
Increased formation of methylglyoxal and protein glycation, oxidation and nitrosation in triosephosphate isomerase deficiency.
TLDR
The increased derangement of MG metabolism and associated glycation, oxidative and nitrosative stress in the propositus may be linked to neurodegenerative process in triosephosphate isomerase deficiency.
Enzymatic deglycation--a new paradigm or an epiphenomenon?
TLDR
Analysis of the fructoselysine 3-phosphate content of haemoglobin from diabetic subjects suggests that, in addition to FN3K, another deglycating mechanism may be operative in human erythrocytes.
Methylglyoxal Can Modify GAPDH Activity and Structure
TLDR
GAPDH can be modified by methylglyoxal intracellular concentrations close to those previously observed in vivo, with measurable changes in isoelectric point and mass, suggesting that conditions associated with elevated intrACEllular MG could modify GAPDH activity in vivo.
The formation of methylglyoxal from triose phosphates
In Krebs-Ringer phosphate buffer, the rate of formation of methylglyoxal from glycerone phosphate and glyceraldehyde 3-phosphate was first order with respect to the triose phosphate with rates
...
1
2
3
4
5
...