Hydroxyurea-mediated regulation of erythrocyte arg

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dc.contributor.author Iyamu, Efe
dc.date.accessioned 2006-05-19T19:49:13Z
dc.date.available 2006-05-19T19:49:13Z
dc.date.issued 2006-05-19T19:49:13Z
dc.identifier.uri http://hdl.handle.net/2271/73
dc.description Clinical Studies I Room G026 Dykes 8:20 AM Abstract 115 en
dc.description.abstract Currently, hydroxyurea (HU), a potent inducer of fetal hemoglobin (Hb F), is the only approved drug for the management of sickle cell disease (SCD).Although the mechanism of induction of Hb F by HU is still unknown, but studies have shown that HU increases Hb F synthesis in response to activation of soluble guanylyl cyclase (sGC), which increases the production of NO. The deficiency in NO due to increased arginase levels may play a role in the pathophysiology of SCD. In this study, we determined the effects of HU on the arginase and nitric oxide synthase (NOS) activities in SCD (N=23) patients and normal control (N = 12) subjects. The results showed that the arginase activity in patients who were on HU therapy were significantly lower than those in SS patients who were not on HU therapy (3.8 ± 1.2 vs 6.6 ± 2.4 U/gHb) and the arginase activity was comparable with those of HbAA volunteers. The NOS activity was higher in patients who were on HU therapy than those who were not on HU therapy (0.72 ± 0.4 vs 0.35 ± 0.15 nmole/ml/min). These data suggest that one of the beneficial effects of HU in vivo may involve the suppression of arginase activity and a concomitant induction of NOS activity, hence an increased production of NO. The outcome of this study may lead to development of improved NO based treatment for SCD. en
dc.description.sponsorship Okolo, Angela Pediatrics en
dc.format.extent 210432 bytes
dc.format.mimetype application/vnd.ms-powerpoint
dc.language.iso en_US en
dc.subject Hydroxyurea en
dc.subject Sickle cell en
dc.title Hydroxyurea-mediated regulation of erythrocyte arg en
dc.type Presentation en

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