The question addresses the protective mechanism seen in individuals who are heterozygous for the sickle-cell allele, specifically how it reduces the frequency and severity of malaria. Let's explore the reasoning behind each of the given options:
This statement is partly accurate. The sickle-cell allele leads to the production of hemoglobin S (HbS) instead of the normal hemoglobin A (HbA). The altered shape of red blood cells in heterozygous individuals (carriers) allows them to carry less oxygen. However, this does not directly inhibit malaria but contributes to the overall environmental stress within the cell.
In sickle cell anemia, the mutation causes a single amino acid substitution (valine replaces glutamic acid) in the beta chain of hemoglobin, leading to abnormal hemoglobin S (HbS). This causes red blood cells to sickle (deform) under low-oxygen conditions. The deformed cells are less hospitable to the malaria parasite, which predominantly invades the normal-shaped red blood cells.
This is not the primary reason. The toxicity of hemoglobin S alone does not directly account for the reduced malaria severity. Instead, it is the environmental stress within the sickle-cell red blood cells that compromises the survival of the malaria parasite.
This statement does not accurately describe the mechanism. In reality, the parasite finds it difficult to thrive and complete its life cycle in the irregular environment of sickle-cell red blood cells, particularly when they deform.
Based on the explanation, the correct answer involves the following aspects:
Therefore, the correct explanations align with these two statements: "Low oxygen binding capacity of hemoglobin" and "Single amino acid substitution in hemoglobin deforms the red blood cells". This unique heterozygosity offers a selective advantage against malaria.