Abstract
Azacitidine is a cytosine analog and antineoplastic agent used in the therapy of myelodysplastic syndromes with mild to moderate liver injuries. Accordingly, this research implicated to evaluate the epigenetic effect of azacytidine on mice liver as a model organism and to determine the role of folic acid administration as a protective methyl donor micronutrient. Thus, forty-eight mice were divided into four groups, reliant on the kind of treatment they received, where animals received calculated doses of azacytidine and folic acid twice a week for three months. Then, animals were killed, and their livers were autopsied and examined for histopathological abnormalities, followed by a genetic assessment for the DNA banding pattern profile of the excised livers. It was found that the anticancer drug azacytidine processes a hepatotoxic effect, and it profoundly modifies the DNA banding pattern. While the combination of folic acid with the administration of azacytidine might induce a protective effect against azacytidine toxic effects, these findings might unravel essential insights and highlight new potential cancer therapeutics.
Highlights
DNA methylation is a molecular epigenetic heritable enzymatic modification, which results from the addition of a methyl group into the carbon-5 of cytosine [1, 2, 3]
This modification plays an essential role in gene expression, where cytosine analogs such as azacytidine could adapt to stress the expression of the genome through changing the methylation pattern and chromatin structure [4, 5, 6]
The DNA methyltransferase (DNMT) inhibitory drug called 5-azacytidine that induces DNA hypomethylation has been used since the 1970s for the treatment of acute leukemia and is still being used as a part of the treatment regimen for Myelodysplastic syndromes (MDS), liver and pancreas cancers [24, 25, 26]
Summary
DNA methylation is a molecular epigenetic heritable enzymatic modification, which results from the addition of a methyl group into the carbon-5 of cytosine [1, 2, 3]. Azacytidine acts to inhibit the action of DNA methyltransferases in the cell, contributing to wide genomic demethylation in tissues [3, 5, 10]. This s-triazine analog was first isolated from the culture filtrate of Streptoverticillium ladakanus and received approval by the U.S.A. Food and Drug Administration (FDA) on May 19, 2004, for the treatment of lymphatic leukemia [11,12].
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