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Abnormal methylation capacity in human liver cirrhosis
A P Geubel1, M C Mairlot, J P Buchet
1Department of Gastroenterology, St-Luc University Hospital, Catholic University of Louvain, Brussels, Belgium.
International Journal of Clinical Pharmacology Research
|January 1, 1988
Summary
Liver cirrhosis impairs the body's methylation capacity, altering arsenic metabolism. Cirrhotic patients excrete less monomethylarsonic acid (MMA) and more dimethylarsinic acid (DMA), indicating methylation pathway dysfunction.
Area of Science:
- Biochemistry
- Toxicology
- Hepatology
Background:
- Methylation is crucial for detoxifying xenobiotics and endogenous compounds.
- Liver cirrhosis significantly impacts metabolic functions.
- Arsenic metabolism involves sequential methylation steps.
Purpose of the Study:
- To assess the impact of liver cirrhosis on methylation capacity.
- To investigate alterations in urinary excretion of methylated arsenic metabolites.
Main Methods:
- Administration of inorganic arsenic to human subjects.
- Measurement of urinary monomethylarsonic acid (MMA) and dimethylarsinic acid (DMA) via atomic absorption spectrometry.
- Comparison of excretion patterns in normal controls, disease controls, and cirrhotic patients.
Main Results:
- Cirrhotic patients showed significantly reduced MMA excretion (4.7%) and increased DMA excretion (40.4%) compared to controls.
- The total percentage of injected arsenic excreted within 24 hours was not affected by cirrhosis.
- Lower MMA levels correlated with impaired liver function (14C aminopyrine breath test).
Conclusions:
- Liver cirrhosis is associated with significant abnormalities in the methylation pathway.
- These methylation defects may affect the metabolism of various substances, including drugs and endogenous compounds.
- Further research is warranted to explore the clinical implications of altered methylation in liver disease.