Abstract

Well established as a ubiquitous enzyme, glucose-6-phosphate dehydrogenase (G6PD) is present in all contemporary organisms and tissues and is conspicuously primeval in evolution. Mandatorily involved in the rate limiting step of the pentose phosphate pathway, its role in averting subsequent cellular insults in assonance to inducing cellular hypertrophy has been well established. While the mechanistic understanding of the G6PD enzyme remains an evolving ground for research, much accent has been laid on its disparity of action in erythrocytes thriving as a tetramer. Of interest, we review the pathologies associated with a consequent deficiency of the enzyme accentuating on favism, infection and drug-mediated hemolytic crisis and finally hemolytic anemia. We culminate the discussion by addressing the lack of empirical evidence in the arena and lay down further prospective research grounds.

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