Sickle cell disease (SCD) is a class of hemoglobinopathy in
humans, which causes a disruption of the normal activities in different
systems. Although this disease begins with the polymerization
of red blood cells during its deoxygenating phase, it can
erupt into a cascade of debilitating conditions such as ischemiareperfusion
injury, inflammation, and painful vaso-occlusion crises.
The purpose of this review is to discuss how these phenomena
can result in the formation of oxidative stress as well as limit
nitric oxide (NO) bioavailability and decrease antioxidant status.
The cumulative effects of these traits cause an increase in other
forms of reactive oxygen species (ROS), which in turn intensify
the symptoms of SCD and generate a vicious circle. Finally, we
will discuss antioxidant therapeutic strategies that limit ROS generation
and subsequently increase NO bioavailability with respect
to endothelial protection in SCD