Exercise and Redox Status Responses Following Alpha-Lipoic Acid Supplementation in G6PD Deficient Individuals.

Kalliopi Georgakouli,Athanasios Jamurtas,Theofanis Tzatzakis,Yiannis Koutedakis,Apostolos Fragkos,Ioannis Fatouros,Konstantinos Papanikolaou,Chariklia Deli

doi:10.3390/antiox7110162

Abstract

G6PD deficiency renders cells more susceptible to oxidative insults, while antioxidant dietary supplementation could restore redox balance and ameliorate exercise-induced oxidative stress. To examine the effects of alpha-lipoic acid (ALA) supplementation on redox status indices in G6PD deficient individuals, eight male adults with G6PD deficiency (D) participated in this randomized double-blind placebo-controlled crossover trial. Participants were randomly assigned to receive ALA (600 mg/day) or placebo for 4 weeks separated by a 4-week washout period. Before and at the end of each treatment period, participants exercised following an exhaustive treadmill exercise protocol. Blood samples were obtained before (at rest), immediately after and 1h after exercise for later analysis of total antioxidant capacity (TAC), uric acid, bilirubin, thiobarbituric acid reactive substances (TBARS) and protein carbonyls (PC). ALA resulted in significantly increased resting TAC and bilirubin concentrations. Moreover, TAC increased immediately and 1h after exercise following both treatment periods, whereas bilirubin increased immediately after and 1h after exercise following only ALA. No significant change in uric acid, TBARS or PC was observed at any time point. ALA supplementation for 4 weeks may enhance antioxidant status in G6PD individuals; however, it does not affect redox responses to acute exercise until exhaustion or exercise performance.

Highlights

Glucose-6-phosphate dehydrogenase (G6PD) enzyme deficiency is the most common enzymopathy, affecting more than 400 million people worldwide [1]
Deficient G6PD activity is well examined in red blood cells (RBC), as it often results in clinical manifestation of mild to severe haemolytic anaemia following exposure to various oxidative agents such as certain drugs [1]
Physical characteristics did not change throughout the study, except for resting heart rate (HR), which decreased following

Summary

Introduction

Glucose-6-phosphate dehydrogenase (G6PD) enzyme deficiency is the most common enzymopathy, affecting more than 400 million people worldwide [1]. G6PD is involved in the generation of NADPH, a reducing agent that participates in various anabolic pathways and the regeneration of reduced glutathione (GSH) [2]. G6PD deficient cells have lower concentrations of GSH. Since GSH protects cells against reactive oxygen species (ROS), G6PD deficiency renders cells susceptible to oxidative stress and its consequences. Deficient G6PD activity is well examined in red blood cells (RBC), as it often results in clinical manifestation of mild to severe haemolytic anaemia following exposure to various oxidative agents such as certain drugs [1]. G6PD deficient activity is present in other cells such as Antioxidants 2018, 7, 162; doi:10.3390/antiox7110162 www.mdpi.com/journal/antioxidants

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