Antioxidant Status and Oxidative Stress in Patients with Chronic ITP

The aim of this study was to establish the antioxidant status and oxidative stress in adult patients with chronic idiopathic thrombocytopenic purpura (ITP). Eighty‐four patients diagnosed with chronic ITP were studied. Fifty‐eight age‐matched healthy subjects were selected as controls. Serum nitrogen monoxide ( NO), oxidized glutathione (GSSG), malondialdehyde (MDA), total antioxidant status (TAS), total oxidant status (TOS), superoxide dismutase(SOD), hydrogen peroxide enzyme (CAT), glutathione peroxidase (GSH‐Px), glutathione (GSH) were evaluated by enzyme‐linked immunosorbent assay (ELISA). It was found that serum SOD, CAT, GSH‐Px, GSH, TAS levels were significantly lower in patients with chronic ITP than controls (all P < 0.05), while serum NO, GSSG, MDA, TOS values were significantly higher (P < 0.05). The number of platelet showed a negative correlation with NO, GSSG, MDA, TOS, respectively,while platelet number showed a positive correlation with SOD, CAT, GSH‐Px, GSH, TAS. These findings suggested that oxidants were increased and antioxidants were decreased in patients with chronic ITP, these may be prominent factors in destructing the platelet membrane. The scavenging of oxygen radical provides a theoretical basis for the treatment of ITP patients.     

Glutathione deficiency intensifies ischaemia‐reperfusion induced cardiac dysfunction and oxidative stress

The efficacy of glutathione (GSH) in protecting ischaemia‐reperfusion (I‐R) induced cardiac dysfunction and myocardial oxidative stress was studied in open‐chest, stunned rat heart model. Female Sprague–Dawley rats were randomly divided into three experimental groups: (1) GSH‐depletion, by injection of buthionine sulphoxamine (BSO, 4 mmol kg^–1, i.p.) 24 h prior to I‐R, (2) BSO injection (4 mmol kg^–1, i.p.) in conjunction with acivicin (AT125, 0.05 mmol kg^–1, i.v.) infusion 1 h prior to I‐R, and (3) control (C), receiving saline treatment. Each group was further divided into I‐R, with surgical occlusion of the main left coronary artery (LCA) for 30 min followed by 20 min reperfusion, and sham. Myocardial GSH content and GSH : glutathione disulphide (GSSG) ratio were decreased by ?50% (P < 0.01) in both BSO and BSO + AT125 vs. C. Ischaemia‐reperfusion suppressed GSH in both left and right ventricles of C (P < 0.01) and left ventricles of BSO and BSO + AT125 (P < 0.05). Contractility (+dP/dt and –dP/dt) in C heart decreased 55% (P < 0.01) after I and recovered 90% after I‐R, whereas ±dP/dt in BSO decreased 57% (P < 0.01) with ischaemia and recovered 76 and 84% (P < 0.05), respectively, after I‐R. For BSO + AT125, ±dP/dt were 64 and 76% (P < 0.01) lower after ischaemia, and recovered only 67 and 61% (P < 0.01) after I‐R. Left ventricular systolic pressure in C, BSO and BSO + AT125 reached 95 (P > 0.05) 87 and 82% (P < 0.05) of their respective sham values after I‐R. Rate‐pressure double product was 11% (P > 0.05) and 25% (P < 0.05) lower in BSO and BSO + AT125, compared with Saline, respectively. BSO and BSO + AT125 rats demonstrated significantly lower liver GSH and heart Mn superoxide dismutase activity than C rats after I‐R. These data indicate that GSH depletion by inhibition of its synthesis and transport can exacerbate cardiac dysfunction inflicted by in vivo I‐R. Part of the aetiology may involve impaired myocardial antioxidant defenses and whole‐body GSH homeostasis.     

Effects of graded exercise-induced dehydration and rehydration on circulatory markers of oxidative stress across the resting and exercising human leg

Exercise in the heat enhances oxidative stress markers in the human circulation, but the contribution of active skeletal muscle and the influence of hydration status remain unknown. To address this question, we measured leg exchange of glutathione (GSH), glutathione disulfide (GSSG), superoxide dismutase activity (SOD) and isoprostanes in seven males at rest and during submaximal one-legged knee extensor exercise in the following four conditions: (1) control euhydration (0% reduction in body mass), (2) mild-dehydration (2%), (3) moderate-dehydration (3.5%), (4) rehydration (0%). In all resting and control exercise conditions, a net GSH uptake was observed across the leg. In contrast, a significant leg release of GSH into the circulation (−354 ± 221 μmol/min, P < 0.05) was observed during exercise with moderate-dehydration, which was still present following full rehydration (−206 ± 122 μmol/min, P < 0.05). During exercise, mild and moderate-dehydration decreased both femoral venous erythrocyte SOD activity (195 ± 6 vs. 180 ± 5 U/L, P < 0.05) and plasma isoprostanes (30 ± 1.1 vs. 25.9 ± 1.3 pg/L, P < 0.05), but during rehydration these were not different from control. In conclusion, these findings suggest that active skeletal muscles release GSH into the circulation under moderate dehydration and subsequent rehydration, possibly to enhance the antioxidant defense.     

Hypoxia preconditioning by cobalt chloride enhances endurance performance and protects skeletal muscles from exercise-induced oxidative damage in rats

Aim: Training under hypoxia has several advantages over normoxic training in terms of enhancing the physical performance. Therefore, we tested the protective effect of hypoxia preconditioning by hypoxia mimetic cobalt chloride against exercise-induced oxidative damage in the skeletal muscles and improvement of physical performance. Method: Male Sprague–Dawley rats were randomly divided into four groups (n = 8), namely control, cobalt-supplemented, training and cobalt with training. The red gastrocnemius muscle was examined for all measurements, viz. free radical generation, lipid peroxidation, muscle damage and antioxidative capacity. Results: Hypoxic preconditioning with cobalt along with training significantly increased physical performance (33%, P < 0.01) in rats compared with training-only rats. Cobalt supplementation activated cellular oxygen sensing system in rat skeletal muscle. It also protected against training-induced oxidative damage as observed by an increase in the GSH/GSSG ratio (36%, P < 0.001; 28%, P < 0.01 respectively) and reduced lipid peroxidation (15%, P < 0.01; 31%, P < 0.01 respectively) in both trained and untrained rats compared with their respective controls. Cobalt supplementation along with training enhanced the expression of antioxidant proteins haem oxygenase-1 (HO-1; 1.2-fold, P < 0.05) and metallothionein (MT; 4.8-fold, P < 0.001) compared with training only. A marked reduction was observed in exercise-induced muscle fibre damage as indicated by decreased necrotic muscle fibre, decreased lipofuscin content of muscle and plasma creatine kinase level (16%, P < 0.01) in rats preconditioned with cobalt. Conclusion: Our study provides strong evidence that hypoxic preconditioning with cobalt chloride enhances physical performance and protects muscle from exercise-induced oxidative damage via GSH, HO-1 and MT-mediated antioxidative capacity.     

Biochemical Markers of Oxidative Stress in Saudi Women with Recurrent Miscarriage

This study was undertaken to investigate the antioxidant/oxidant status in recurrent miscarriage patients. Antioxidants including glutathione peroxidase (GPx), catalase (CAT), glutathione reductase (GR), reduced glutathione (GSH) and selenium (Se), as well as the oxidants hydrogen peroxide (H₂O₂), oxidised glutathione (GSSG) and lipid peroxidation were assayed in plasma, whole blood and placental tissue of non-pregnant women (NP), healthy pregnant women (HP), and recurrent miscarriage (RM) patients. Results indicated that all antioxidant activities and levels in plasma and whole blood of HP women were consistently moderately lower, and much more significantly lower in RM patients when both were compared to those seen in NP women (P<0.05 and P<0.001, respectively). Furthermore, whereas plasma antioxidant activities and levels were significantly lower in RM patients, those of whole blood and placental tissue were much more significantly lower when compared with HP women (P<0.001). Concurrent with these findings there were consistent increases of equal statistical significance and magnitude in the levels of all investigated oxidants assayed in all samples when compared in between subjects of the study as indicated above. Data thus illustrated a distinct shift in favor of oxidative reactions and reactive oxygen species (ROS) generation, and very significant decreases in the GSH/GSSG ratios in whole blood and placental tissue of RM patients when compared to HP and NP women (P<0.001). The above noted oxidative stress could have been a major causative factor of recurrent miscarriage.     

The effect of whole-body cryostimulation on the prooxidant–antioxidant balance in blood of elite kayakers after training

The effect of whole-body cryostimulation prior to kayak training on the prooxidant-antioxidant balance was evaluated and compared to the effect of a single cryostimulation treatment in untrained men. The kayakers underwent a ten-day training cycle with pre-training daily whole-body cryostimulation for three min (temperature: –120 to –140°C) and training without cryostimulation as a control. Blood samples were obtained before and after the sixth and the tenth day of training and from the untrained men before and 20 min after cryostimulation. In untrained men cryostimulation induced an increase in the activity of superoxide dismutase (SOD) by 36% (P < 0.001) and glutathione peroxidase (GPx) by 68% (P < 0.01) in the erythrocytes and an increase in the conjugated dienes (CD) in plasma by 36% (P < 0.05) and in the erythrocytes by 71% (P < 0.001). In the kayakers comparing both types of training after the sixth day, the level of CD in plasma was 46 (P < 0.001) and 40% (P < 0.01) lower in erythrocytes, and the concentration of thiobarbituric acid-reactive substances in plasma was 24% (P < 0.05) lower with pre-training cryostimulation. After the sixth day of training with cryostimulation, SOD activity was also 47% (P < 0.001) lower, while GPx activity after the tenth day was reduced by more than 50% (P < 0.01) as compared to control training. Whole-body cryostimulation per se stimulates the generation of reactive oxygen species. Yet, the oxidative stress induced by kayak training was reduced by prior exposure to extremely low temperatures.     

Cardiac hypertrophy alters myocardial response to ischaemia and reperfusion in vivo

The impact of cardiac hypertrophy on myocardial biochemical and physiological responses to ischaemia-reperfusion (I-R) was investigated in vivo. Hypertrophy was produced by aortic constriction (PH) or swimming training (TH). Open-chest rat hearts in PH, TH and a sedentary control group (SC) were subjected: (1) to ischaemia, by surgical occlusion of the main descending branch of the left coronary artery for 30 min; (2) to I-R, by releasing the occluded blood vessel for 15 min; or (3) to a sham operation. Ischaemia per se had little effect on heart oxidative and antioxidant status, or lipid peroxidation. However, I-R significantly decreased glutathione (GSH) content, increased glutathione disulfide (GSSG) content, and reduced GSH/GSSG ratio in the SC hearts. These alterations were associated with decreased activities of GSH peroxidase and GSSG reductase, and an increase in lipid peroxidation. Myocardial ATP, total adenine nucleotide content and energy charge in SC were significantly decreased after ischaemia, whereas levels of purine nucleotide derivatives, particularly adenosine, were elevated. No significant alteration of GSH status or adenine nucleotide metabolism occurred after ischaemia or I-R in hypertrophied hearts. In bodi PH and TH, glutathione content was significantly higher than in SC, whereas activities of GSH peroxidase and GSSG reductase were lower. TH rats maintained a higher heart rate (HR), peak systolic pressure, and energy charge during I-R. These data indicate that hypertrophied but well-functioned hearts may be more resistant to I-R induced disturbances of myocardial oxidative and antioxidant functions.     

Evaluation of Oxidative Stress and Antioxidant Status in Chronic Obstructive Pulmonary Disease

Chronic obstructive pulmonary disease (COPD) is a common respiratory condition involving the airways and characterized by airflow limitation. Gaseous and noxious particles play an important role in this process. Antioxidants are the substances that may protect cells from the damage caused by unstable molecules known as free radicals. The increased oxidative stress in patients with COPD is the result of an increased burden of inhaled oxidants, as well as increased amounts of reactive oxygen species (ROS) generated by various inflammatory, immune and epithelial cells of the airways. A total of 150 subjects with COPD and 100 healthy controls subjects were enrolled in this study from the period October 2015 to January 2016. The investigation included measurements of plasma superoxide dismutase activity (SOD), catalase activity (CAT), glutathione content (GSH) reduced form, (GPx) glutathione peroxidase, glutathione reductase (GR) and lipid peroxidation (LPO). Absorbance was measured by UV spectrophotometer. The estimated values of SOD, catalase, GPx, GSH and GR were found to be significantly (P = 0.0001) lower among the cases compared with controls. But, the levels of MDA were higher (P = 0.0001) in cases as compared to control group and there was significant difference in the oxidative stress parameters among the various stages of COPD. The post hoc analysis revealed that SOD was significantly (P < 0.01) lower among the mild, moderate and severe patients compared with very severe patients. The catalase was also observed to be significantly (P = 0.01) lower among mild, moderate and severe patients than very severe patients. The GPx was found to be significantly (P = 0.002) lower among the mild, moderate and severe patients compared with very severe patients. MDA was observed to be significantly higher in mild, moderate and severe patients compared with very severe (P = 0.001). GR was significantly (P = 0.003) lower among mild, moderate and severe patients than very severe patients. However, there was no significant difference in GSH among severity of COPD patients. This study suggests that oxidant and antioxidant imbalance plays an important role in various stages of severity of COPD. These results revealed the presence of an oxidative stress in subjects with COPD, and it is proportionate to the severity of disease.     

Oxidative stress and changes in liver antioxidant enzymes induced by experimental dicroceliosis in hamsters

The purpose of our study was to assess the effects of experimental dicroceliosis on the antioxidant defense capability of the liver in hamsters. Studies were carried out at 80 and 120 days after infection with an oral dose of 40 metacercariae of Dicrocoelium dendriticum. The parasitic pathology was ascertained by the presence of fluke eggs in feces, increased serum ALT and AST activities, and histological findings. The concentration of thiobarbituric acid-reactive substances (TBARS) and the ratio of oxidized to reduced glutathione (GSSG/GSH), measured as markers of oxidative stress, were significantly increased [TBARS: +40% and +84% at 80 and 120 days postinfection (p.i.), respectively; GSSG/GSH: +200% and +117%]. Dicroceliosis increased Se-dependent glutathione peroxidase (GPx) activity in both cytosol (+24% and +46%) and mitochondria (+73% and +41%). Superoxide dismutase activity was significantly reduced in cytosol (−19% and −38%) and mitochondria (−20% and −39%). No significant change was found in the activity of Se-independent GPx or catalase. The ratio of glutathione peroxidase/glutathione reductase at 80 and 120 days p.i. was increased by 25% and 63%, respectively. Gamma-glutamyl cysteinyl synthetase activity was increased by 27% and 20%, respectively. Our data indicate that although dicroceliosis courses with activation of antioxidant enzymes and glutathione synthesis, inefficient scavenging of reactive oxygen species takes place, resulting in oxidative liver damage. Received: 1 November 1998 / Accepted: 17 December 1998     

Glutathione-dependent modulation of exhausting exercise-induced changes in neutrophil function of rats

Reduced glutathione (GSH) plays a central role in maintaining an effective synergism between various physiological and exogenous antioxidants. We tested the effects of GSH andN-acetylcysteine (NAC, a pro-GSH clinical drug), intraperitoneal (i.p.) supplementation and GSH deficiency on exercise-induced leucocyte margination and neutrophil oxidative burst activity. GSH, NAC (1g · kg^–1) or placebo saline was i.p. injected (one or eight times) to male rats (n seven per group). The GSH-deficient rats were prepared by i.p. injections ofl-buthionine-[SR]-sulphoximine (BSO, 6 mmol · 1^–1 · kg^–1) twice daily for 4 days. Exercised animals were subjected to treadmill run to exhaustion. Exhausting treadmill exercise significantly decreased peripheral blood leucocyte count in the controls (P < 0.001). Such exercise-associated leucocyte margination was prevented by GSH supplementation. Peripheral blood neutrophil counts were significantly higher (P < 0.02) in the GSH-supplemented groups compared to the placebo control groups. Exercise-induced increase in peripheral blood neutrophil oxidative burst activity as measured by luminol-enhanced chemiluminescence per volume of blood tended to be higher in the GSH-supplemented group (P < 0.10), and lower in the GSH-deficient rats (P < 0.02). In these experiments, for the first time we have shown that GSH supplementation can induce neutrophil mobilization and decrease exercise-induced leucocyte margination, and that exogenous and endogenous GSH can regulate exercise-induced stimulation of the neutrophil oxidative burst.     

Exercise training reduces oxidative stress in people living with HIV/AIDS: a pilot study

Background: Exercise training has been shown to be an effective strategy to balance oxidative stress status; however, this is underexplored in people living with HIV/AIDS (PLWHA).

Objective: To evaluate the effects of exercise training on oxidative stress in PLWHA receiving antiretroviral therapy.

Methods: Patients performed 24 sessions (3 times per week, 8 weeks) of either aerobic (AT), resistance (RT), or concurrent training (CT). Glutathione disulphide to glutathione ratio (GSSG/GSH) in circulating erythrocytes and thiobarbituric acid–reactive substances (TBARS) in plasma samples were assessed as oxidative stress markers. Eight PLWAH completed the training protocol (AT =3, RT =3, CT =2). The GSSG/GSH and TBARS values were logarithmically transformed to approximate a normal distribution. A paired t-test was used to determine the differences between baseline and post-training values.

Results: Data-pooled analysis showed a decrease in GSSG/GSH and TBARS after the training period: log GSSG/GSH= –1.26?±?0.57 versus –1.54?±?0.65, p?=?.01 and log TBARS =0.73?±?0.35 versus 0.43?±?0.21, p?=?.01. This was paralleled by a rise in peak oxygen uptake (VO_2peak?=?29.14?±?5.34 versus 32.48?±?5.75?ml kg^?1 min^?1, p?=?.04). All the subjects who performed resistance exercises showed an average gain of 37?±?8% in muscle strength with no difference between performing single or multiple sets in terms of muscle strength gain. The results reinforce the clinical importance of exercise as a rehabilitation intervention for PLWHA and emphasizes the safety of exercise at the physiological level with the potential to mediate health outcomes.     

Seasonal variation in antioxidant enzyme activity in seminal plasma in Holstein bulls

Seminal oxidative stress status is emerging as a significant prognostic tool in assisted reproductive technology. A dynamic interplay between pro- and anti-antioxidant substances in the ejaculate is essential. In this study, we determined seasonal changes in the activity of the antioxidant enzyme defence system comprising catalase (CAT), glutathione peroxidase (GPx) and superoxide dismutase (SOD) in seminal plasma (SP) of mature Holstein bull’s semen. Samples were collected by a bovine artificial vagina from 30 sexually mature Holstein bulls, and CAT, GPx and SOD activities were determined for different seasons. The CAT enzymatic activity determined in SP was greater in autumn as compared with other seasons (P < 0.01). Significantly lower GPx activity was found in winter compared with other seasons (62 ± 12 versus 133 ± 35; P < 0.01). However, SOD was not significantly affected by the season. The results reported confirm the influence of season on sperm quality. Furthermore, this study presents convincing evidence that SP composition is important in determining the antioxidant defence system of ejaculated spermatozoa.     

Responses of rat myocardial antioxidant defences and heat shock protein HSP72 induced by 12 and 24‐week treadmill training

Aim: The purpose of this study was to determine the effects of both a short (12 weeks) and a long‐term (24 weeks) endurance treadmill‐training programme on the levels of oxidative stress markers, the activity of the enzymatic antioxidants, and the content of the 72 kDa heat shock protein (HSP72) in rat myocardium. Methods: Thirty male Wistar rats were randomly assigned to exercise trained (n = 16) and sedentary (n = 14) groups. After 12 week of training, eight rats were killed while the remaining eight continued the training programme until 24 week. Results: Seven sedentary controls were killed together with each trained group. Levels of thiobarbituric acid‐reactive substances (TBARS), protein carbonyls, and total and oxidized glutathione (tGSH and GSSG) in myocardial homogenates were unchanged by training irrespective of the protocol duration. However, an increased content of the oxidative stress biomarkers was detected in hearts from both the 24‐week trained rats and their sedentary controls when compared with their corresponding 12‐week groups. The antioxidant enzymatic activities total and mitochondrial superoxide dismutase (tSOD and mtSOD, respectively), glutathione peroxidase (GPX) and glutathione reductase (GR), remained unchanged after the 12‐week training period whereas a significant increase in tSOD and mtSOD activities (18%, P < 0.05) was observed in heart homogenates of 24‐week trained animals as compared with their sedentary controls. HSP72 expression levels were not significantly modified after 12 week of training but a threefold increase was detected after 24 week (P < 0.05). Conclusion: These results demonstrate that a long‐term endurance training (24 weeks) induced discrete increases in antioxidant enzyme activities in rat myocardium and elicited a marked enhancement in HSP72 expression levels. However, a shorter training programme (12 weeks), was not effective in increasing heart antioxidant defences.     

Short-term exercise training improves diaphragm antioxidant capacity and endurance

These experiments tested the hypothesis that short-term endurance exercise training would rapidly improve (within 5 days) the diaphragm oxidative/antioxidant capacity and protect the diaphragm against contraction-induced oxidative stress. To test this postulate, male Sprague-Dawley rats (6 weeks old) ran on a motorized treadmill for 5 consecutive days (40–60 min · day⁻¹) at approximately 65% maximal oxygen uptake. Costal diaphragm strips were excised from both sedentary control (CON, n=14) and trained (TR, n=13) animals 24 h after the last exercise session, for measurement of in vitro contraction properties and selected biochemical parameters of oxidative/antioxidant capacity. Training did not alter diaphragm force-frequency characteristics over a full range of submaximal and maximal stimulation frequencies (P > 0.05). In contrast, training improved diaphragm resistance to fatigue as contraction forces were better-maintained by the diaphragms of the TR animals during a submaximal 60-min fatigue protocol (P < 0.05). Following the fatigue protocol, diaphragm strips from the TR animals contained 30% lower concentrations of lipid hydroperoxides compared to CON (P < 0.05). Biochemical analysis revealed that exercise training increased diaphragm oxidative and antioxidant capacity (citrate synthase activity +18%, catalase activity +24%, total superoxide dismutase activity +20%, glutathione concentration +10%) (P < 0.05). These data indicate that short-term exercise training can rapidly elevate oxidative capacity as well as enzymatic and non-enzymatic antioxidant defenses in the diaphragm. Furthermore, this up-regulation in antioxidant defenses would be accompanied by a reduction in contraction-induced lipid peroxidation and an increased fatigue resistance. Accepted: 6 August 1999     

Glutathione in gingival crevicular fluid and its relation to local antioxidant capacity in periodontal health and disease

Aims: To determine possible changes in gingival crevicular fluid (GCF) antioxidant defence in chronic adult periodontal disease and to investigate the nature of the local radical scavenging mechanisms, with particular reference to glutathione.

Methods: GCF and plasma were collected from patients with chronic periodontitis and age and sex matched control subjects (n = 10). Polymorphonuclear leucocytes (PMNLs) were prepared and gingival epithelial cells (GECs) were collected by conventional methods from periodontally healthy subjects. PMNL were stimulated with F-Met-Leu-Phe after cytochalasin B treatment. Enhanced chemiluminescence was used to determine the total antioxidant capacity and to investigate the activity of cell fractions and reducing agents. GCF concentrations of reduced (GSH) and oxidised (GSSG) glutathione were determined by high performance liquid chromatography.

Results: Plasma and GCF from patients contained lower mean (SD) total antioxidant capacity (501.8 (123) μM Teq/litre and 658.3 (392) μM Teq/litre, respectively) compared with controls (577.9 (99.8) and 1351.5 (861) μM Teq/litre, respectively). Antioxidant light recovery profiles for GCF demonstrated a stepped response, not seen in plasma, which was inhibited by N-ethylmaleimide. This response was also detected in the cytosolic fraction of GEC and anaerobically stimulated PMNL. Similar antioxidant profiles, inhibitable by N-ethylmaleimide, were obtained with cysteamine, cysteine, and GSH. Control GCF contained high mean (SD) concentrations of glutathione (GSH, 1899.8 (494.4)μM; GSSG, 256.8 (152.4)μM). GCF from patients with periodontitis contained significantly lower amounts of GSH (mean, 1183.1; SD, 580.3μM) and GSSG (mean, 150.1; SD, 44.9μM).

Conclusions: GSH values and total antioxidant capacity are reduced in chronic periodontal disease. The high concentrations of GSH present in GCF in health are similar to those found extracellularly in the lung and may represent an important antioxidant and anti-inflammatory defence strategy common to exposed epithelial surfaces.

     

Serum oxidant and antioxidant status during early and late recovery periods following an all-out 21-km run in trained adolescent runners

It is well documented that intense exercise precipitates oxidative stress in adults. However, there is lack of related studies concerning oxidant and antioxidant status during early and late recovery periods in adolescent athletes, following endurance exercise in particular. This study investigated aspects of the serum oxidant and antioxidant status of 12 male adolescent (16.2 ± 0.6 years) trained runners during early and late recovery periods after an all-out 21-km run. Venous blood samples were taken immediately before, 2 and 4 h following (early recovery period), and 24 h following (late recovery period) the 21-km run. Samples were analyzed for serum concentrations of thiobarbituric acid-reactive substances (TBARS), uric acid (UA), reduced glutathione (GSH), and enzymatic activity of xanthine oxidase (XO), superoxide dismutase (SOD), and catalase (CAT). During the early recovery period, there were increases in the 4-h GSH (194.8 ± 10.4 vs. 211.8 ± 11.4 mg l⁻¹, P < 0.05), 2- and 4-h UA (307.8 ± 68.6 vs. 327.4 ± 63.8; 330.2 ± 65.1 μmol l⁻¹, P < 0.05), and 2-h CAT (2.05 ± 0.44 vs. 3.07 ± 0.51 U ml⁻¹, P < 0.05), and decreases in the 2-h XO (11.1 ± 1.5 vs. 10.3 ± 1.2 U l⁻¹, P < 0.05) compared to the corresponding pre-exercise level, respectively. No change was observed in SOD (P > 0.05). At the late recovery period, there was an increase in CAT (2.80 ± 0.49 U ml⁻¹, P < 0.05) and TBARS (2.99 ± 0.83 vs. 4.40 ± 1.38 nmol ml⁻¹, P < 0.05). These data indicate that although the antioxidant capacity of adolescent runners is augmented during the early recovery period following the 21-km run, they were not completely protected from oxidative stress during the later recovery period.     

Temporal association of elevations in serum cardiac troponin T and myocardial oxidative stress after prolonged exercise in rats

The objective of this study was to determine if prolonged exercise resulted in the appearance of cardiac troponin T (cTnT) in serum and whether this was associated with elevated levels of myocardial oxidative stress. Forty-five male Sprague–Dawley rats were randomized into four groups and killed before (PRE-EX), immediately (0HR), 2 (2HR) and 24 h (24HR) after a 3-h bout of swimming with 5% body weight attached to their tail. In all animals serum cTnT was assayed using 3rd generation electrochemiluminescence. In homogenized heart tissue myocardial malondialdehyde (MDA), a marker of lipid peroxidation, glutathione (GSH), and a non-enzymatic estimate of total antioxidant capacity (T-AOC) were assessed spectrophotometrically. At PRE-EX cTnT was undetectable in all animals. At 0HR (median, range: 0.055, 0.020–0.100) and 2HR post-exercise (0.036, 0.016–2.110) cTnT was detectable in all animals (P < 0.05). At 24HR post-exercise cTnT was undetectable in all animals. An elevation in MDA was observed 0HR (mean ± SD: 1.7 ± 0.2 nmol mgpro⁻¹) and 2HR (1.6 ± 0.3 nmol mgpro⁻¹) post-exercise compared with PRE-EX (1.3 ± 0.2 nmol mgpro⁻¹; P < 0.05). The antioxidant response to this challenge was a significant (P < 0.05) decrease in GSH 2HR and 24HR post-exercise. Despite this T-AOC did not alter across the trial (P > 0.05). The results indicated that prolonged and strenuous exercise in rats resulted in an elevation in cTnT, a biomarker of cardiomyocyte damage, in all animals 0HR and 2HR after exercise completion. The time course of cTnT elevation was temporally associated with evidence of increased lipid peroxidation in the rat heart.     

Influence of intense exercise on saliva glutathione in prepubescent and pubescent boys

Intense aerobic exercise has been found to prompt changes in oxidative stress, but in children remains almost unexplored. The aim was to investigate the effect of intense physical exercise on reduced glutathione (GSH as a biomarker of oxidative stress) and adrenocortical response (to verify a certain level of stress after exercise) in 38 prepubescent and 32 pubescent non-athlete boys. Four subgroups were established as puberty stage and physical fitness. Saliva samples were taken before and after incremental exercise testing to measure GSH, and cortisol levels. Saliva reduced glutathione levels were lower in all subgroups after exercise except in the prepubescent average fit group, significance being greater in the pubescent (P < 0.001) than in the prepubescent group (P < 0.01). Saliva cortisol increased after exercise in all except in the prepubescent “average fit” group. Physical exercise may give rise to oxidative stress and adrenocortical response in pubescent and prepubescent boys, depending on the duration and intensity of the test.     

Effects of exercise‐induced intracellular acidosis on the phosphocreatine recovery kinetics: a 31P MRS study in three muscle groups in humans

Little is known about the metabolic differences that exist among different muscle groups within the same subjects. Therefore, we used ³¹P‐magnetic resonance spectroscopy (³¹P‐MRS) to investigate muscle oxidative capacity and the potential effects of pH on PCr recovery kinetics between muscles of different phenotypes (quadriceps (Q), finger (FF) and plantar flexors (PF)) in the same cohort of 16 untrained adults. The estimated muscle oxidative capacity was lower in Q (29 ± 12 mM min^‐1, CV_{inter‐subject} = 42%) as compared with PF (46 ± 20 mM min^‐1, CV_{inter‐subject} = 44%) and tended to be higher in FF (43 ± 35 mM min^‐1, CV_{inter‐subject} = 80%). The coefficient of variation (CV) of oxidative capacity between muscles within the group was 59 ± 24%. PCr recovery time constant was correlated with end‐exercise pH in Q (p < 0.01), FF (p < 0.05) and PF (p <0.05) as well as proton efflux rate in FF (p < 0.01), PF (p < 0.01) and Q (p = 0.12). We also observed a steeper slope of the relationship between end‐exercise acidosis and PCr recovery kinetics in FF compared with either PF or Q muscles. Overall, this study supports the concept of skeletal muscle heterogeneity by revealing a comparable inter‐ and intra‐individual variability in oxidative capacity across three skeletal muscles in untrained individuals. These findings also indicate that the sensitivity of mitochondrial respiration to the inhibition associated with cytosolic acidosis is greater in the finger flexor muscles compared with locomotor muscles, which might be related to differences in permeability in the mitochondrial membrane and, to some extent, to proton efflux rates. Copyright © 2013 John Wiley & Sons, Ltd.     

Altered glutathione redox state in schizophrenia

Altered antioxidant status has been reported in schizophrenia. The glutathione (GSH) redox system is important for reducing oxidative stress. GSH, a radical scavenger, is converted to oxidized glutathione (GSSG) through glutathione peroxidase (GPx), and converted back to GSH by glutathione reductase (GR). Measurements of GSH, GSSG and its related enzymatic reactions are thus important for evaluating the redox and antioxidant status. In the present study, levels of GSH, GSSG, GPx and GR were assessed in the caudate region of postmortem brains from schizophrenic patients and control subjects (with and without other psychiatric disorders). Significantly lower levels of GSH, GPx, and GR were found in schizophrenic group than in control groups without any psychiatric disorders. Concomitantly, a decreased GSH:GSSG ratio was also found in schizophrenic group. Moreover, both GSSG and GR levels were significantly and inversely correlated to age of schizophrenic patients, but not control subjects. No significant differences were found in any GSH redox measures between control subjects and individuals with other types of psychiatric disorders. There were, however, positive correlations between GSH and GPx, GSH and GR, as well as GPx and GR levels in control subjects without psychiatric disorders. These positive correlations suggest a dynamic state is kept in check during the redox coupling under normal conditions. By contrast, lack of such correlations in schizophrenia point to a disturbance of redox coupling mechanisms in the antioxidant defense system, possibly resulting from a decreased level of GSH as well as age-related decreases of GSSG and GR activities.