L-Cysteine supplementation protects the erythrocyte glucose-6-phosphate dehydrogenase activity from reduction induced by forced training Kleopatra H. Schulpis a , George J. Reclos b , Theodore Parthimos c , Nickolaos Parthimos c , Andreas Gavriilidis d , Stylianos Tsakiris c, ⁎ a Institute of Child Health, Research Center, “Aghia Sophia” ChildrenTs Hospital, GR-11527 Athens, Greece b R and D Diagnostics, 33 Alevizatou, 15561 Athens, Greece c Department of Experimental Physiology, Medical School, University of Athens, PO Box 65257, GR-15401 Athens, Greece d Department of Physical Education and Sport Science, University of Athens, Greece Received 7 April 2006; received in revised form 8 June 2006; accepted 21 June 2006 Available online 12 July 2006 Abstract Background: L-Cysteine (L-cys) is implicated in the reduction of free radical production. Aim: To investigate the effect of training and L-cys supplementation on the erythrocyte glucose-6-phosphate dehydrogenase (G6PD) activity. Methods: Blood was obtained from 10 basketball players pre-game (group A), post-game (group B) and after 1 week on L-cys (0.5 g/24 h orally) supplementation pre- (group C) and post-training (group D). Total antioxidant status (TAS) and G6PD activity were evaluated with commercial kits. Results: TAS increased in the groups with L-cys addition (group C and group D). Post-exercise, TAS and G6PD activity were remarkably higher (1.48 ± 0.12 mmol/L, 8.9 ± 1.7 U/g Hb, respectively) in group D than those in group B (0.92 ± 0.10 mmol/L, 4.8 ± 1.6 U/g Hb, p <0.01). G6PD activity positively correlated with TAS (r = 0.70, p < 0.001 pre- and r = 0.61, p < 0.001 post-training) in all the studied groups. Conclusions: G6PD activity is lowered by training probably due to free radical action. L-cys supplementation may protect G6PD activity from reduction by increasing total antioxidant capacity and glutathione production. G6PD activity should be evaluated in the blood of athletes of Mediterranean origin and female G6PD-deficient heterozygotes. © 2006 The Canadian Society of Clinical Chemists. All rights reserved. Keywords: G6PD; Oxidation; Free radicals; Cysteine; Exercise Introduction Glucose-6-phosphate dehydrogenase (G6PD) deficiency is one of the most common, X-linked genetic disease affecting an estimated 400 million people worldwide. In Greece, where this disease is endemic, an estimated 225,000 males and 92,000 females are affected [1]. Hematological problems arising in G6PD-deficient populations through exposure to oxidizing xenobiotics have been well characterized, ranging from hemolysis of red blood cells and hereditary non-spherocytic hemolytic anemia, to sepsis and life threatening kernicterus in the newborn [2,3]. In Greece, G6PD deficiency is the main cause of severe neonatal jaundice [1]. Population studies conducted in several parts of the country have shown an uneven distribution of G6PD ranging from 1% to 30% in male infants [2]. The Mediterranean variant of the G6PD mutation results in almost total enzyme deficiency mainly affecting people from Greece, Southern Italy and Sardinia [2]. G6PD is the first enzyme in the pentose phosphate pathway. Its most important function is to reduce nicotinamide adenine dinucleotide phosphate (NADP) to NADPH [4]. NADPH is required as a cofactor in the reduction of oxidized glutathione Clinical Biochemistry 39 (2006) 1002 – 1006 ⁎ Corresponding author. Fax: +30 2107462571. E-mail address: stsakir@cc.uoa.gr (S. Tsakiris). 0009-9120/$ - see front matter © 2006 The Canadian Society of Clinical Chemists. All rights reserved. doi:10.1016/j.clinbiochem.2006.06.006