Sickle Cell Anemia Lab Report

In this experimental lab we studied the differences between sickle-cell trait, sickle cell anemia, and normal hemoglobin. Two allelic forms of hemoglobin were separated, normal HbA and the form found in people with sickle cell disease, HbS. When hemoglobin from people with severe sickle cell anemia, sickle cell trait, and normal red blood cells was subjected to electrophoresis, the previous results on figure A were obtained. Substitution mutations that result in the replacement of one amino acid by another with a different electrical charge can lead to changes in the overall charges of the protein. Protein electrophoresis was used to detect allelic variation. When the electrical field is applied, many proteins have a net negative charge

It was clear that the hemoglobin molecules of individuals with sickle cell anemia migrated at a different rate, and thus ended up at a different place on the gel, from the hemoglobin of normal individuals. Individuals with sickle cell trait had about half normal and half sickle cell hemoglobin, each type making up half of the contents of the heme groups in any red blood cell. Substitution mutations that result in the replacement of one amino acid by another with a different electrical charge can lead to changes in the overall charges of the protein. Amino acids consist of an amino and a carboxyl group bound to the same carbon atom and a side chain that specifies for the 20 different amino acids present in our proteins. Amino or carboxyl groups in the side chain make the amino acid either basic or acidic. These amino acids affect the isoelectric point. Both sickle-cell hemoglobin and normal hemoglobin are acidic, therefore, have lower isoelectric

With respect to the sickle cell (HbS), the molecular nature is a substitution of valine for glutamic acid at the sixth amino acid position in the β-globin gene. Hemoglobin is the main substance of the red blood cell. It helps red blood cells carry oxygen from the air in our lungs to our whole body. Normal red blood cells contain hemoglobin A. Individuals with sickle cell conditions make a different abnormal form of hemoglobin A called hemoglobin S. Red blood cells that contain mostly hemoglobin S do not live as long as normal red blood cells. These red blood cells become sickle-shaped and have difficulty passing through small blood vessels. When sickle-shaped cells block small blood vessels, less blood can reach that part of the body. If the tissue does not receive a normal blood flow it eventually becomes damaged. The abnormal hemoglobin HbS is inherited from the parents of the individual, who may be carriers with either sickle cell trait or parents with sickle cell disease. If an individual inherits only on sickle cell gene, then that individual carries the sickle-cell trait. Sickle-cell trait carries one HbS producing gene inherited from the parents and one HbA gene. However, if the individual inherits two sickle cell genes then they have sickle cell disease. Although sickle-cells are destroyed rapidly in the body of individuals with the disease, causing anemia and the