scholarly journals A Short-Term Resistance Training Circuit Improved Antioxidants in Sedentary Adults with Down Syndrome

2021 ◽  
Vol 2021 ◽  
pp. 1-6
Author(s):  
M. Rosety-Rodriguez ◽  
M. Bernardi ◽  
S. Elosegui ◽  
I. Rosety ◽  
A. J. Diaz ◽  
...  
Keyword(s):  
Down Syndrome ◽  
Resistance Training ◽  
Oxidative Damage ◽  
Glutathione Reductase ◽  
Reductase Activity ◽  
Community Support ◽  
Knee Extensors ◽  
Antioxidant Defence ◽  
Defence System ◽  
Antioxidant Defence System

Previous studies have found aerobic training improved oxidative damage in people with Down syndrome (DS). However, there is a lack of information regarding the influence of resistance training on redox imbalance in this population. Accordingly, this study was conducted to determine the effect of resistance training (RT) on antioxidant defence system in sedentary adults with DS. Thirty-six male adults with DS were recruited through different community support groups. Eighteen were randomly assigned to perform a circuit RT program with 6 stations, 3 days/week for 12 weeks. Plasma total antioxidant status (TAS), reduced glutathione (GHS), ascorbate, serum α-tocopherol, and erythrocyte glutathione reductase activity were assessed. Plasma malondialdehyde (MDA) and carbonyl groups (CG) were assessed as markers of oxidative damage. Muscle strength was also measured. Dynamic torque of knee extensors and flexors as well as maximal handgrip strength was significantly improved after the completion of the training program. Plasma levels of TAS and erythrocyte glutathione reductase (GR) activity were significantly increased. Conversely, MDA and CG levels were significantly reduced. It was concluded RT improved antioxidant defence system and reduced oxidative damage in adults with DS. Further, long-term studies are required to determine whether the increased antioxidant system may improve clinical outcomes of adults with DS.

Effect of salt stress on antioxidant defence system in soybean root nodules

1998 ◽  
Vol 25 (6) ◽  
pp. 665 ◽  
Author(s):  
María E. Comba ◽  
María P. Benavides ◽  
María L. Tomaro
Keyword(s):  
Superoxide Dismutase ◽  
Antioxidant Enzymes ◽  
Glutathione Reductase ◽  
Ascorbate Peroxidase ◽  
Reduced Glutathione ◽  
Nitrogenase Activity ◽  
Reductase Activity ◽  
Saline Stress ◽  
Antioxidant Defence ◽  
Antioxidant Defence System

The antioxidant defence systems of soybean (Glycine max (L.) Merr) nodules responded differently to 50 and 200 mM NaCl. At 50 mM NaCl, leghaemoglobin content and nitrogenase activity remained unaltered but there was an overall increase in the antioxidant enzymes (ascorbate peroxidase, catalase, glutathione reductase and superoxide dismutase) and in reduced glutathione. After returning the salinised nodules to a non-saline environment (recovery), the enzymatic activities returned to the initial values but reduced glutathione remained high with respect to the controls measured at the end of the experiment (final controls). Severe salt treatment reduced the leghaemoglobin content and nitrogenase activity by 31% and 50%, respectively. Ascorbate peroxidase, catalase and glutathione reductase activities decreased between 30 and 100% while superoxide dismutase and reduced glutathione increased over the controls by 19% and 30% respectively. After recovery, glutathione reductase increased over the final controls and reduced glutathione remained as under 50 mM NaCl. Malondialdehyde content and total protein remained unchanged in nodules treated with the two salt concentrations. These results suggest that under mild saline stress, the elevated levels of the antioxidant enzymes and reduced glutathione protect nodules against the activated oxygen species thus avoiding lipid and protein peroxidation, and leghaemoglobin breakdown. However, severe saline treatment produced an irreversible decay in the leghaemoglobin content and nitrogenase activity despite the high reduced glutathione level and glutathione reductase activity.

scholarly journals Downregulation of FeSOD-A expression in Leishmania infantum alters trivalent antimony and miltefosine susceptibility

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Ana Maria Murta Santi ◽  
Paula Alves Silva ◽  
Isabella Fernandes Martins Santos ◽  
Silvane Maria Fonseca Murta
Keyword(s):  
Oxidative Stress ◽  
Western Blot ◽  
Leishmania Infantum ◽  
Transcript Level ◽  
Drug Susceptibility ◽  
Central Component ◽  
Multiplication Rate ◽  
Antioxidant Defence ◽  
Defence System ◽  
Antioxidant Defence System

Abstract Background Superoxide dismutase (SOD), a central component of the antioxidant defence system of most organisms, removes excess superoxide anions by converting them to oxygen and hydrogen peroxide. As iron (Fe) SOD is absent in the human host, this enzyme is a promising molecular target for drug development against trypanosomatids. Results We obtained Leishmania infantum mutant clones with lower FeSOD-A expression and investigated their phenotypes. Our attempts to delete this enzyme-coding gene using three different methodologies (conventional allelic replacement or two different CRISPR/methods) failed, as FeSOD-A gene copies were probably retained by aneuploidy or gene amplification. Promastigote forms of WT and mutant parasites were used in quantitative reverse-transcription polymerase chain reaction (RT-qPCR) and western blot analyses, and these parasite forms were also used to assess drug susceptibility. RT-qPCR and western blot analyses revealed that FeSOD-A transcript and protein levels were lower in FeSOD-A−/−/+L. infantum mutant clones than in the wild-type (WT) parasite. The decrease in FeSOD-A expression in L. infantum did not interfere with the parasite growth or susceptibility to amphotericin B. Surprisingly, FeSOD-A−/−/+L. infantum mutant clones were 1.5- to 2.0-fold more resistant to trivalent antimony and 2.4- to 2.7-fold more resistant to miltefosine. To investigate whether the decrease in FeSOD-A expression was compensated by other enzymes, the transcript levels of five FeSODs and six enzymes from the antioxidant defence system were assessed by RT-qPCR. The transcript level of the enzyme ascorbate peroxidase increased in both the FeSOD-A−/−/+ mutants tested. The FeSOD-A−/−/+ mutant parasites were 1.4- to 1.75-fold less tolerant to oxidative stress generated by menadione. Infection analysis using THP-1 macrophages showed that 72 h post-infection, the number of infected macrophages and their intracellular multiplication rate were lower in the FeSOD-A−/−/+ mutant clones than in the WT parasite. Conclusions The unsuccessful attempts to delete FeSOD-A suggest that this gene is essential in L. infantum. This enzyme plays an important role in the defence against oxidative stress and infectivity in THP-1 macrophages. FeSOD-A-deficient L. infantum parasites deregulate their metabolic pathways related to antimony and miltefosine resistance. Graphic Abstract

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