Glucose-6-phosphate dehydrogenase deficiency links to malaria resistance, not antibiotics, via Plasmodium’s reliance on the hexose monophosphate shunt.

This assertion-reason question from biology exams tests G6PD deficiency’s protective role against malaria parasites in RBCs, clarifying misconceptions about antibiotic resistance.

Question Breakdown

Assertion A claims Glucose-6-phosphate dehydrogenase (G6PD) deficiency associates with antibiotic resistance, which is inaccurate—it’s actually tied to increased infection risk or malaria protection. Reason R correctly notes Plasmodium depends on the hexose monophosphate shunt (HMS, or pentose phosphate pathway) and reduced glutathione (GSH) for growth in red blood cells (RBCs), as the parasite lacks these pathways fully.

Option Analysis

• Both A and R correct, R explains A: Incorrect. A is false; no evidence links G6PD deficiency to antibiotic resistance—in fact, it may heighten bacterial susceptibility due to impaired neutrophil function.

• Both A and R correct, R does not explain A: Wrong. A remains false.

• A correct, R incorrect: False. A lacks support; R is true, as G6PD generates NADPH for GSH, starving Plasmodium of antioxidants in deficient RBCs.

• A incorrect, R correct: Correct. G6PD deficiency confers malaria resistance (not antibiotics) precisely because R explains the mechanism: oxidative stress kills parasites reliant on host HMS/GSH.

Correct Answer

A is not correct but R is correct. This aligns with standard medical and exam interpretations.​

G6PD Deficiency Overview

Glucose-6-phosphate dehydrogenase deficiency disrupts the hexose monophosphate shunt, impairing NADPH and GSH production in RBCs, leading to hemolysis under oxidative stress. Common in malaria-endemic areas, it evolved as protection against Plasmodium, not antibiotics.

Assertion A: No Antibiotic Link

A wrongly ties G6PD deficiency to antibiotic resistance. Studies show deficient patients face higher infection risks from bacteria/fungi due to weak ROS/NET production in neutrophils, not resistance. Antibiotics like sulfa drugs trigger hemolysis in G6PD patients.

Reason R: Plasmodium’s RBC Dependence

Plasmodium depends on hexose monophosphate shunt and reduced glutathione for detoxifying RBC oxidants during growth. In G6PD-deficient cells, low GSH causes oxidative damage, halting parasite development—heterozygotes show 2-80x lower infection rates.

Why R Doesn’t Explain A

R explains malaria resistance, a classic balanced polymorphism. Antibiotic claims stem from infection triggers (fever/oxidants), not resistance.

Exam Tips for Biochemistry

For GATE/CUET:

• Recall: G6PD first HMS enzyme; deficiency = favism/malaria hedge.

• Spot distractors: “Antibiotic” vs. “malarial” resistance.