background: bilirubin encephalopathy is a clinical syndrome, associated with bilirubin toxicity in the central nervous system, resulting in chronic and permanent sequelae. it has been estimated that approximately 60% and 80% of term and preterm newborns develop jaundice in the first week of life, respectively. in the present study, we aimed to determine the prevalence, morbidity, and mortality ...

Glucose-6-phosphate dehydrogenase (G6PD, EC1.1.1.49) is expressed in all tissues where it is the first and rate-limiting enzyme of the pentose phosphate pathway (PPP) [1] that consists of the oxidative and non-oxidative branches and usually works at 1–2% of its maximal potential in healthy subjects due to the high level of nicotinamide adenine dinucleotide phosphate (NADPH). The G6PD gene is wi...

Glucose-6-phosphate dehydrogenase (G6PD) deficiency is characterized by the loss of NADPH and enhanced erythrocyte oxidant sensitivity. Historically, it has been theorized that the elevated oxidant sensitivity of G6PD-deficient erythrocytes arises as the direct consequence of decreased intracellular glutathione (GSH) concentrations. To directly investigate the basis of G6PD deficiency oxidant s...

Oxidative and osmotic stress have been implicated in the pathogenesis of cataracts. Reactive oxygen intermediates (ROI) mediate peroxidation of membrane lipids and cause irreversible damage to lens proteins. The purpose of this study was to assess the changes in erythrocyte glucose- 6-phosphate dehydrogenase enzyme (G6PD) and reduced glutathione (GSH) levels in the development of senile and dia...

Extreme hyperbilirubinemia (EHB) caused by neonatal glucose-6-phosphate dehydrogenase (G6PD) deficiency is strongly associated with mortality and long-term neurodevelopmental impairment, yet there are limited national strategies to reduce this burden in South Asia. Current known and predicted prevalence of G6PD deficiency in Afghanistan, Bangladesh, Bhutan, India, Nepal, and Pakistan ranges fro...

G lucose-6-phosphate dehydrogenase (G6PD) deficiency is a common Xlinked human enzyme defect (1). There are a few reports that link G6PD deficiency to diabetes (2–4). We undertook a cross-sectional study at Maccabi Healthcare Services, an Israeli HMO serving two million members. All interactions and information are captured on an electronic medical record. Our study population included all male...

The vascular endothelium compensates for oxidant stress by increasing the activity of antioxidant enzymes such as glucose-6-phophate dehydrogenase (G6PD). G6PD provides reducing equivalents of NAPDH to maintain glutathione stores and modulates nitric oxide synthase (eNOS) activity. To determine whether deficient G6PD activity perturbs these responses, we treated bovine aortic endothelial cells ...

We recently demonstrated that a 17-ketosteroid, epiandrosterone, attenuates L-type Ca(2+) currents (I(Ca-L)) in cardiac myocytes and inhibits myocardial contractility. Because 17-ketosteroids are known to inhibit glucose-6-phosphate dehydrogenase (G6PD), the rate-limiting enzyme in the pentose phosphate pathway, and to reduce intracellular NADPH levels, we hypothesized that inhibition of G6PD c...

BIOCHEMISTRY AND NATURAL HISTORY OF G6PD DEFICIENCY G6PD is an enzyme in the pentose phosphate pathway, a metabolic pathway that supplies reducing energy to cells, in particular erythrocytes, by maintaining the level of nicotinamide adenine dinucleotide phosphate (NADPH). NADPH in turn maintains the level of glutathione that helps protect erythrocytes against oxidative damage. In states of oxid...

Glucose-6-phosphate dehydrogenase (G6PD) deficient subjects are vulnerable to oxidative stress. Quercetin, a flavonoids, has been employed as a potent oxygen-free radical scavenger in order to assess the protective effects of quercetin against H2O2-induced oxidative damage in G6PD-deficient and normal human erythrocytes. Erythrocytes of G6PD-deficient (n = 10) and normal (n = 10) subjects were ...