Related Experiment Videos
Hyperhomocysteinemia and macromolecule modifications in uremic patients
Alessandra F Perna1, Rosanna Capasso, Cinzia Lombardi
1First Division of Nephrology, School of Medicine, Second University of Naples, Naples, Italy. alessandra.perna@unina2.it
Clinical Chemistry and Laboratory Medicine
|October 4, 2005
Summary
Hyperhomocysteinemia in chronic kidney disease patients damages DNA and proteins. Folate treatment can lower homocysteine levels and improve these molecular changes.
Area of Science:
- Biochemistry
- Nephrology
- Molecular Biology
Background:
- Hyperhomocysteinemia is common in chronic renal failure and uremia.
- Mechanisms of homocysteine toxicity in uremia, particularly cardiovascular effects, are under investigation.
Purpose of the Study:
- To investigate the molecular damage to DNA and proteins caused by hyperhomocysteinemia in uremic patients.
- To explore the potential of folate treatment in mitigating these effects.
Main Methods:
- Analysis of DNA methylation status in mononuclear cells.
- Assessment of protein modifications, including oxidative damage and isopeptide bond formation.
- Evaluation of folate's impact on homocysteine levels and macromolecular changes.
Main Results:
- Hyperhomocysteinemia in uremic patients leads to DNA hypomethylation.
- Proteins are damaged through oxidative modifications and formation of homocysteine thiolactone-induced isopeptide bonds.
- Folate treatment partially reduces homocysteine levels and improves macromolecular alterations.
Conclusions:
- Both DNA and proteins undergo structural modifications in uremia due to elevated homocysteine.
- These macromolecular changes are implicated in the clinical complications of hyperhomocysteinemia in renal patients.