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Md. Fahim Ahmad, Mohd. Owais Ansari, Nuzhat Parveen, Shoeb Ahmad, Sana Jameel and *G. G. H. A. Shadab


Hydroxyurea (HU) is an antineoplastic drug. It has widespread usage
in the treatment of both malignant and nonmalignant diseases like
Sickle-cell anaemia and HIV infections. It acts on the enzyme
ribonucleotide reductase to inhibit the conversion of ribonucleotides
into deoxyribonucleotides, thereby limiting DNA biosynthesis. The
principal use of HU has been as a myelosuppressive agent in the
treatment of myeloproliferative syndromes, particularly chronic
myelogenous leukemia and polycythemia vera. Although treatment of
chronic myelogenous leukemia with HU for many years has been
reserved for patients whose disease was no long irresponsive to
busulfan. HU acts as a cytotoxic and antineoplastic agent that
specifically affects the S phase and interrupts the cell cycle in the G2 and S phases. Studies
showed that HU causes rapid cell death through the initiation of uncontrolled free radical
chain reaction. Free radical reactions are able to devastate cellular metabolism quickly by
inactivating enzymes, cross-linking DNA and altering membrane function through lipid autooxidation.
Despite being very frequently used in the treatment of several malignant and nonmalignant
diseases, prolonged use of HU has been reported to cause mutation and clastogenic
effects in several in vitro systems, as well as cytogenetic damage in exposed mice. It has also
shown a wide variety of toxic effects, like induction of chromosomal aberrations and
cytotoxicity, as well as a well established genotoxic activity in cell culture and rodent models.

Keywords: Hydroxyurea, antineoplastic drug, ribonucleotide reductase, cytotoxic, genotoxic.

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