Final answer:
G6PD deficiency leads to a shortened lifespan of the enzyme, which is critical for protecting red blood cells. Symptoms include neonatal jaundice and acute hemolytic anemia, but the genetic mutation offers some protection against malaria.
Step-by-step explanation:
True, Glucose-6-phosphate dehydrogenase (G6PD) deficiency is a genetic disorder characterized by a reduced half-life of the G6PD enzyme. This enzyme is crucial for the pentose phosphate pathway, which helps protect red blood cells from oxidative damage by maintaining levels of glutathione.
Due to the deficiency, individuals have lower levels of G6PD, leading to heightened susceptibility to anemia because of the faster breakdown of red blood cells, especially when exposed to certain foods, drugs, or stressors.
Patients with G6PD deficiency, most often males due to the X-linked pattern of inheritance, exhibit symptoms such as prolonged neonatal jaundice and are at risk for episodes of acute hemolytic anemia in response to various oxidative stressors. Interestingly, this genetic trait offers a protective advantage against malaria, which historically has been a significant advantage in endemic areas.