Final answer:
G6PD deficiency is inherited in an X-linked recessive manner, affecting primarily males but also potentially affecting female carriers due to lyonization. The condition is characterized by a deficiency in the G6PD enzyme which is crucial in protecting red blood cells against oxidative damage.
Step-by-step explanation:
Mode of Inheritance of G6PD Deficiency
The mode of inheritance of G6PD deficiency is X-linked recessive. This means that the gene causing G6PD deficiency is located on the X chromosome. Males have one X and one Y chromosome, so if their single X chromosome carries the mutation, they will express the disease. Females have two X chromosomes, and the disease will typically only manifest in them if they are homozygous for the mutation, having received one mutated gene from each parent. However, due to a process called lyonization, where random inactivation of an X chromosome in certain cells happens, female carriers can have a population of G6PD deficient red cells, causing them to show symptoms of the deficiency as well.
While the majority of patients with G6PD deficiency are male, female carriers can be clinically affected due to lyonization. Individuals with G6PD deficiency have abnormally low levels of the G6PD enzyme, which plays a crucial role in the pentose phosphate pathway by maintaining levels of NADPH and thus protecting red blood cells against oxidative damage. Another interesting aspect of this condition is that individuals who are homozygous for the G6PD mutation are less prone to malaria, suggesting that in regions where malaria is endemic, the mutation could confer a selective advantage.