Glucose-6-phosphate dehydrogenase – from oxidative stress to cellular functions and degenerative diseases

Abstract

Glucose-6-phosphate dehydrogenase (G6PD), the first and rate-limiting enzyme of the pentose phosphate pathway, is indispensable to maintenance of the cytosolic pool of NADPH and thus the cellular redox balance. The role of G6PD as an antioxidant enzyme has been recognized in erythrocytes for a long time, as its deficiency is associated with neonatal jaundice, drug- or infection-mediated hemolytic crisis, favism and, less commonly, chronic non-spherocytic hemolytic anemia. To a large extent, advances in the field were made on the pathophysiology of G6PD-deficient erythrocytes, and the molecular characterization of different G6PD variants. Not until recently did numerous studies cast light on the importance of G6PD in other aspects of the physiology of both cells and organisms. Deficiency in G6PD activity, and hence a disturbance in redox homeostasis, can lead to dysregulation of cell growth and signaling, anomalous embryonic development, altered susceptibility to viral infection as well as increased susceptibility to degenerative diseases. The present review covers recent developments in this field. Additionally, molecular characterization of G6PD variants, especially those frequently found in Taiwan and Southern China, is also addressed.

Effect of a 12-Week Training Program on Levels of Glucose-6-Phosphate Dehydrogenase and Antioxidant Activity

“…These adaptations may result from cumulative effects of repeated exercise bouts on the gene expression of antioxidant enzymes as on exercise-induced modulation of antioxidant defence (13,14). In conclusion we suggest that regular, long-term physical exercise cause adaptations in antioxidant defences.…”

The effects of superoxide dismutase knockout on the oxidative stress parameters and survival of mouse erythrocyt

“…The role of the regeneration of glutathione in the protection of erythrocytes against redox-cycling xenobiotics generating oxidative stress is evident in favism. In this case, an inborn deficiency of glucose 6-phosphate dehydrogenase activity leads to erythrocyte destruction upon exposure to fava beans or certain drugs [1,2]. By contrast, no significant anomalies in physiological erythrocyte functions have been reported in acatalasemia [3,4] and glutathione reductase deficiency [4].…”

Impact of Diabetes Mellitus Type 2 in the Activity of Glucose-6-Phosphate Dehydrogenase in Human Erythrocyte

“…NADPH is important for the removal of ROS and prevention of cell damage [37,38]. ROS is stimulated by high glucose levels, which damages the nucleus by linking with DNA and RNA.…”