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Kharbanda, K.K. et al.

Kharbanda, Rogers, Mailliard, Siford, Barak, Beckenhauer, Sorrell, Tuma,

Role of elevated S-adenosylhomocysteine in rat hepatocyte apoptosis: protection by betaine.

Previous studies from our laboratory have shown that ethanol consumption results in an increase in hepatocellular S-adenosylhomocysteine levels. Because S-adenosylhomocysteine is a potent inhibitor of methylation reactions, we propose that increased intracellular S-adenosylhomocysteine levels could be a major contributor to ethanol-induced pathologies. To test this hypothesis, hepatocytes isolated from rat livers were grown on collagen-coated plates in Williams' medium E containing 5% FCS and exposed to varying concentrations of adenosine in order to increase intracellular S-adenosylhomocysteine levels. We observed increases in caspase-3 activity following exposure to adenosine. This increase in caspase activity correlated with increases in intracellular S-adenosylhomocysteine levels and DNA hypoploidy. The adenosine-induced changes could be significantly attenuated by betaine administration. The mechanism of betaine action appeared to be via the methylation reaction catalyzed by betaine-homocysteine-methyltransferase. To conclude, our results indicate that the elevation of S-adenosylhomocysteine levels in the liver by ethanol is a major factor in altering methylation reactions and in increasing apoptosis in the liver. We conclude that ethanol-induced alteration in methionine metabolic pathways may play a crucial role in the pathologies associated with alcoholic liver injury and that betaine administration may have beneficial therapeutic effects.[1]

References

Role of elevated S-adenosylhomocysteine in rat hepatocyte apoptosis: protection by betaine. Kharbanda, K.K., Rogers, D.D., Mailliard, M.E., Siford, G.L., Barak, A.J., Beckenhauer, H.C., Sorrell, M.F., Tuma, D.J. Biochem. Pharmacol. (2005) [Pubmed]

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