Oxidative Stress in Sickle Cell Disease Associated Priapism

SCD is a hemoglobinopathy resulting from the expression of abnormal sickle hemoglobin (HbS), which leads to red blood cell rigidity. Abnormal red blood cells are associated with poor blood flow resulting in tissue hypoxia and ischemia [98]. In addition to hemoglobinopathy and red blood cell sickling, SCD features an independent spectrum of vascular dysfunction, involving abnormalities in NO bioavailability, enhanced responses to vasoconstrictors, and elevated oxidative stress [99, 100].

Priapism is a very common vasculopathy of SCD. This erection disorder consists of nonwillful, excessive, and often recurrent penile erection unrelated to sexual excitement. It afflicts about 40% of men with SCD [101, 102]. Ischemic priapism, the most common form of priapism in which blood flow in the corpora cavernosa is absent, is frequently associated with irreversible penile tissue necrosis, as well as permanent and irreversible ED [102-111].

The sources of ROS in the penis and the mechanism of ROS-mediated pathophys-iology associated with priapism remain mostly unknown. One study recently reported increased lipid peroxidation and increased protein oxidation in corporal tissue of rats with priapism and in SCD mice [112]. Unpublished results obtained in our laboratory implicate eNOS uncoupling and NADPH oxidase as sources of ROS in the penis of SCD transgenic mice (Musicki and Burnett, unpublished). Future studies are warranted to examine the sources of ROS and the effect of oxidative stress on downstream signaling in the penis in SCD-associated priapism.

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