G6PD Deficiency: Exploring the Relationship with Different Medical Disorders

Abstract

G6PD deficiency (G6PDD) is associated with oxidative stress resulting from an imbalance between reactive oxygen species (ROS) production and the body's ability to counteract. In this review, we explore the adverse effects of G6PDD on diverse physiological processes and disease outcomes. Past studies have demonstrated the association between G6PDD and various other diseases, indicating a link between G6PDD to heightened oxidative stress by accelerating virus replication, worsening infection severity, and weakening the body's defense mechanisms. Such stress is critical in the destruction of red blood cells (RBCs) during infections and has a detrimental impact on redox signaling, ultimately impacting cell health and promoting cancer development. Furthermore, it impairs endothelial function by lowering the nitric oxide (NO) level and increasing stress, resulting in detrimental cardiac consequences and reduced myocardial antioxidant capacity. Because ROS contributes to inflammation, this imbalance causes conditions such as early atherosclerosis. It also compromises the functionality of NO-regulated bronchodilators and conditions such as G6PDD exacerbate the risks of kidney damage. Elevated ROS levels can also induce harm in retinal tissues, blood vessels, brain cells, and Beta-cells, hence quickening the progression of diseases like Diabetic Retinopathy. Furthermore, oxidative stress plays a significant role in cerebral ischemic pathogenesis, contributing to neurodegenerative disorders. Additionally, decreased NADPH level is vital for NO synthesis as it can impact blood vessel relaxation and can potentially lead to ischaemic priapism. Investigating the association between G6PDD and other medical conditions is crucial as it helps to identify possible approaches to mitigate oxidative stress, thereby preventing associated complications and diseases, particularly in situations where current treatment options are insufficient.