Sickle cell anemia is an inherited disorder in which red blood cells become stiff and sickle-shaped. This condition is caused by defective hemoglobin that clusters together, forming long, rod-like structures. The abnormal red blood cells cannot freely move through small blood vessels and thus cause blockages that deprive organs and tissues of oxygen. A study published in 2003 established that the use of hydroxyurea therapy decreases mortality among sickle cell patients by forty percent and significantly reduces pain and acute chest crises. Hydroxyurea produces an increase of fetal hemoglobin, which prevents the polymerization of sickle hemoglobin. It is also a source of nitric oxide (NO), a messenger molecule needed to maintain normal blood flow and pressure. Hydroxyurea reacts with hemoglobin by first forming a nitroxide radical. It then undergoes a series of reactions to produce the nitric oxide needed to increase fetal hemoglobin. Although the production of NO can proceed through various pathways, the process always requires the removal of the hydrogen atom from the OH group of hydroxyurea. Read More

• Medicine
• Chemistry