Final answer:
G6PD deficiency is inherited in an 1. X-linked recessive manner, predominantly affecting males and causing symptoms like prolonged neonatal jaundice due to the crucial role of G6PD in the pentose phosphate pathway and prevention of oxidative damage in red blood cells.
Step-by-step explanation:
The mode of inheritance of G6PD deficiency is X-linked recessive. This means that the condition is linked to a gene on the X chromosome. As males have only one X chromosome, they are almost exclusively the patients displaying full manifestations of G6PD deficiency. Females can be carriers and may experience symptoms due to lyonization, which is a random inactivation of one of the X chromosomes. This creates a mixed population of normal and G6PD deficient red blood cells within the same individual. Severe cases can occur in homozygous females, though this is rare. G6PD deficiency can lead to various symptoms, including prolonged neonatal jaundice.
G6PD is crucial as it participates in the pentose phosphate pathway, which aids in maintaining the level of NADPH and thus protects red blood cells against oxidative damage. The deficiency of this enzyme can lead to the premature breakdown of red blood cells, resulting in anemia.
X-linked recessive inheritance is often observed in other conditions as well, such as color blindness and hemophilia. With this form of inheritance, female offspring of carrier mothers have a 50% chance of being carriers themselves, while male offspring have a 50% chance of being affected by the disease.