• Age-related responses in circulating markers of redox status in healthy adolescents and adults during the course of a training macrocycle

      Zalavras, A; Fatouros, IG; Deli, CK; Draganidis, D; Theodorou, AA; Soulas, D; Koutsioras, Y; Koutedakis, Y; Jamurtas, AZ; Department of Physical Education & Sport Science, University of Thessaly, Karies, 42100 Trikala, Greece. (Hindawi, 2015-04-06)
      Redox status changes during an annual training cycle in young and adult track and field athletes and possible differences between the two age groups were assessed. Forty-six individuals (24 children and 22 adults) were assigned to four groups: trained adolescents, (TAD, N=13), untrained adolescents (UAD, N=11), trained adults (TA, N=12), and untrained adults (UA, N=10). Aerobic capacity and redox status related variables [total antioxidant capacity (TAC), glutathione (GSH), catalase activity, TBARS, protein carbonyls (PC), uric acid, and bilirubin] were assessed at rest and in response to a time-trial bout before training, at mid- and posttraining. TAC, catalase activity, TBARS, PC, uric acid, and bilirubin increased and GSH declined in all groups in response to acute exercise independent of training status and age. Training improved aerobic capacity, TAC, and GSH at rest and in response to exercise. Age affected basal and exercise-induced responses since adults demonstrated a greater TAC and GSH levels at rest and a greater rise of TBARS, protein carbonyls, and TAC and decline of GSH in response to exercise. Catalase activity, uric acid, and bilirubin responses were comparable among groups. These results suggest that acute exercise, age, and training modulate the antioxidant reserves of the body.
    • Antioxidant responses following active and passive smoking of tobacco and electronic cigarettes

      Poulianiti, Konstantina; Karatzaferi, Christina; Flouris, Andreas D; Fatouros, Ioannis G; Koutedakis, Yiannis; Jamurtas, Athanasios Z (Taylor & Francis, 2016-07-27)
      It has been indicated that acute active and passive tobacco cigarette smoking may cause changes on redox status balance that may result in significant pathologies. However, no study has evaluated the effects of active and passive e-cigarette smoking on redox status of consumers.
    • Antioxidants and AP-1 activation: a brief overview.

      Gómez del Arco, Pablo; Martínez-Martínez, Sara; Calvo, Victor; Armesilla, Angel; Redondo, Juan Miguel (Elsevier BV, 1997)
      Activity of the transcription factor AP-1 is controlled by different MAPK cascades that regulate the different AP-1 components at the transcriptional and posttranscriptional level. Recently, AP-1 has been shown to behave as a redox-sensitive transcription factor that can be induced under both pro-oxidative and antioxidative conditions. In this overview we summarize the signaling pathways that converge on the activation of AP-1 and the components of these pathways that have been shown to be targets of antioxidants. The activation of AP-1 by antioxidants may account for the expression of a number of genes that mediate important functions under physiological conditions.
    • Exercise-induced oxidative stress in G6PD-deficient individuals.

      Nikolaidis, Michalis G.; Jamurtas, Athanasios Z.; Paschalis, Vassilis; Kostaropoulos, Iason A.; Kladi-Skandali, Athina; Balamitsi, Vera; Koutedakis, Yiannis; Kouretas, Dimitris (Lippincott Williams & Wilkins, 2006)
      PURPOSE: This study was designed to investigate whether individuals with glucose-6-phosphate dehydrogenase (G6PD) deficiency can exercise without greater perturbations in their redox status compared with non-G6PD-deficient individuals. METHODS: Nine males with established G6PD deficiency and nine males with normal G6PD activity performed two exhaustive treadmill exercise protocols of different duration (the shorter one lasting 12 min and the longer one 50 min). Several hematological parameters, reduced glutathione (GSH), oxidized glutathione (GSSG), thiobarbituric acid reactive substances (TBARS), protein carbonyls, catalase, and total antioxidant capacity (TAC) were measured in the blood before and after each exercise bout. RESULTS: Both GSH and GSSG were significantly higher in the control group compared with the G6PD-deficient group at baseline (0.404 +/- 0.101 vs 0.195 +/- 0.049 mmol.L(-1) for GSH and 0.047 +/- 0.012 vs 0.012 +/- 0.006 mmol.L(-1) for GSSG; P < 0.05); as a result, their ratio was not significantly different between the two groups (P > 0.05). All other oxidative stress indices were not different between groups at rest (P > 0.05). Exercise of both durations affected significantly (P < 0.05) and similarly the levels of all oxidative stress indices either in the G6PD-deficient group or in the control group. Only the long exercise affected GSH status significantly (P < 0.05), whereas both short and long exercise increased the levels of TBARS, protein carbonyls, catalase activity, and TAC to a similar extent (P < 0.05). CONCLUSION: G6PD-deficient individuals are able to exercise until exhaustion without higher oxidative stress compared with non-G6PD-deficient individuals. Exercise duration is an important determinant of the magnitude of exercise-induced changes for GSH, GSSG, and GSH/GSSG, but not for TBARS, protein carbonyls, catalase activity, or TAC.
    • JNK (c-Jun NH2-terminal kinase) is a target for antioxidants in T lymphocytes.

      Gómez del Arco, Pablo; Martínez-Martínez, Sara; Calvo, Victor; Armesilla, Angel; Redondo, Juan Miguel (American Society for Biochemistry and Molecular Biology, 1996-10-18)
      AP-1 has been shown to behave as a redox-sensitive transcription factor that can be activated by both oxidant and antioxidant stimuli. However, the mechanisms involved in the activation of AP-1 by antioxidants are largely unknown. In this study we show that the structurally unrelated antioxidant agents pyrrolidine dithiocarbamate (PDTC), butylated hydroxyanisole, and Nacetylcysteine activated JNK (c-Jun NH2-terminal kinase) in Jurkat T cells. This activation differed substantially from that mediated by phorbol 12-myristate 13-acetate (PMA) and Ca2+ ionophore or produced by costimulation with antibodies against the T cell receptor-CD3 complex and to CD28. The activation of JNK by classical T cell stimuli was transient, whereas that mediated by PDTC and butylated hydroxyanisole (but not N-acetylcysteine) was sustained. The kinetics of JNK activation correlated with the expression of c-jun which was transient after stimulation with PMA plus ionophore and prolonged in response to PDTC, which also transiently induced c-fos. In addition, JNK activation by PMA plus ionophore was sensitive to inhibitors of signaling pathways involving Ca2+, protein kinase C, and tyrosine phosphorylation, which failed to inhibit the activation mediated by PDTC. Transfection of trans-dominant negative expression vectors of ras and raf, together with AP-1-dependent reporter constructs, as well as Western blot analysis using anti-ERK (extracellular signal-regulated kinase) antibodies, indicated that the Ras/Raf/ERK pathway did not appear to mediate the effect of the antioxidant. However, the combined treatment with PDTC and PMA, two agents that synergize on AP-1 activation, resulted in the persistent phosphorylation of ERK-2. In conclusion, our results identify JNK as a target of antioxidant agents which can be regulated differentially under oxidant and antioxidant conditions.
    • Systemic Redox Imbalance in Chronic Kidney Disease: A Systematic Review.

      Poulianiti, Konstantina P; Kaltsatou, Antonia; Mitrou, Georgia I; Jamurtas, Athanasios Z; Koutedakis, Yiannis; Maridaki, Maria; Stefanidis, Ioannis; Sakkas, Giorgos K; Karatzaferi, Christina (Hindawi, 2016-06-07)
      Patients with chronic kidney disease (CKD) experience imbalance between oxygen reactive species (ROS) production and antioxidant defenses leading to cell and tissue damage. However, it remains unclear at which stage of renal insufficiency the redox imbalance becomes more profound. The aim of this systematic review was to provide an update on recent advances in our understanding of how the redox status changes in the progression of renal disease from predialysis stages 1 to 4 to end stage 5 and whether the various treatments and dialysis modalities influence the redox balance. A systematic review was conducted searching PubMed and Scopus by using the Cochrane and PRISMA guidelines. In total, thirty-nine studies met the inclusion criteria and were reviewed. Even from an early stage, imbalance in redox status is evident and as the kidney function worsens it becomes more profound. Hemodialysis therapy per se seems to negatively influence the redox status by the elevation of lipid peroxidation markers, protein carbonylation, and impairing erythrocyte antioxidant defense. However, other dialysis modalities do not so far appear to confer advantages. Supplementation with antioxidants might assist and should be considered as an early intervention to halt premature atherogenesis development at an early stage of CKD.
    • The influence of vitamin E succinate on the stability of polyethylene oxide PEO controlled release matrix tablets.

      Shojaee, Saeed; Cumming, Iain; Kaialy, Waseem; Nokhodchi, Ali (Elsevier, 2013-11-01)
      Hydrophilic matrices are a principal technology used for extended release (ER) oral dosage forms and a recent review concluded that their development is currently one of the most important challenges in pharmaceutical research. High molecular weight polyethylene oxides (PEOs) have been proposed as an alternative to hydroxypropylmethylcellulose (HPMC) for the manufacture of controlled release matrix tablets. It is known that PEO's are prone to oxidative degradation which can occur by chain scission and can be catalyzed by metal ions. In this study, we investigated the stability of PEO matrix tablets, of different molecular weight, containing diltiazem hydrochloride, when stored at 40 °C. The results show that there were dramatic increases in the release rate of the diltiazem following storage over only a few weeks, resulting in immediate release profiles after eight weeks, even for the highest molecular weight grade. We employed Gel permeation chromatography (GPC), viscosity and differential scanning calorimetry (DSC) techniques to try and determine the underlying causes of these dramatic shifts in dissolution profiles on storage. The results showed that there were significant decreases in the molecular weight of the PEO's during storage. The second part of the study looked at the addition of three different levels of vitamin E succinate to the tablets. The results clearly demonstrate the ability of the added antioxidant to reverse the significant reductions in molecular weight seen using GPC, viscosity and DSC. Importantly the addition of the antioxidant was able to stabilize the release profile of the diltiazem especially when present at a 1% level. Researchers and those working in pharmaceutical development should be aware of the potential stability risks when making matrix tablets containing PEO's and may wish to consider the addition of an antioxidant to the tablet formulation.
    • Vitamin E correlates inversely with non-transferrin-bound iron in sickle cell disease.

      Marwah, S.S.; Wheelwright, D.; Blann, A.D.; Rea, C.; Beresford, R.; Phillips, Jonathan D.; Wright, J.; Bareford, D. (Wiley InterScience, 2001)
      Decreased serum vitamin E levels are found in homozygous sickle cell disease (SCD). Excessive transfusions may lead high non-transferrin-bound iron (NTBI). Hypothesizing a relationship between the two, vitamin E (measured using high performance liquid chromatography) was significantly lower in 30 SCD patients than in 30 age-/sex-matched controls (P < 0.001), but NTBI (bleomycin assay) was higher (P < 0.001). Vitamin E was lower in 10 transfused patients than in 20 non-transfused patients (P < 0.001) with a significant inverse correlation between the NTBI and vitamin E (r = -0.58, P < 0.001). NTBI associated with iron overload in SCD may increase the potential for oxidative damage and low vitamin E activity may compound this effect.