What is the effect of sickle cell anemia on hemoglobin proteins?

Sickle cell anemia is a genetic disorder that affects the structure of hemoglobin, the protein responsible for transporting oxygen in the blood. In individuals with this condition, a mutation occurs in the gene that codes for the beta globin subunit of hemoglobin. This mutation causes the hemoglobin molecules to polymerize under low oxygen conditions, leading them to distort into a rigid, crescent or "sickle" shape.

The sickle-shaped cells are less flexible and can obstruct blood flow in the small blood vessels, which can lead to pain and organ damage, as well as a reduction in the cells’ ability to effectively carry oxygen. This shape change directly impacts the function and lifespan of red blood cells, as they are more susceptible to breakdown and can lead to anemia.

In contrast to the other options, sickle cell anemia does not involve hemoglobin becoming more stable or increasing in size, nor does it lead to the complete disappearance of hemoglobin from the bloodstream. The primary effect is indeed the change to a sickle shape, which clearly demonstrates how a single mutation in the hemoglobin gene can have widespread effects on health.