Antioxidant effect of diphenyl diselenide on oxidative stress caused by acute physical exercise in skeletal muscle and lungs of mice

2009 ◽  
Vol 27 (4) ◽  
pp. 216-222 ◽  
Author(s):  
Marina Prigol ◽  
Cristiane Luchese ◽  
Cristina Wayne Nogueira
2007 ◽  
Vol 32 (2) ◽  
pp. 190-196 ◽  
Author(s):  
José Alexandre Bachur ◽  
Sérgio Britto Garcia ◽  
Hélio Vannucchi ◽  
Alceu Afonso Jordao ◽  
Paula Garcia Chiarello ◽  
...  

The objective of this study was to analyze the oxidative stress of skeletal muscle of sedentary rats at the morphological and biochemical level, due to acute physical effort performed at different intensities and during different periods of time. Forty-two male sedentary Wistar rats were divided into two groups, group A (swimming for 50 min) and group B (swimming for 100 min), which were further subdivided into 3 different exercise intensities, non-weight bearing (subgroup I), 3% weight load (subgroup II), and 5% weighted load (subgroup III), as well as a control-rested group (C). The animals were killed by ether inhalation and fragments of the gastrocnemius muscle were removed for the determination of malondialdehyde (MDA), reduced glutathione (GSH), and vitamin E concentrations. When all groups were compared with the control-rested group (C), gastrocnemius MDA levels at 50 and 100 min were higher at all swimming intensities. GSH consumption was greater at all intensities in group A, and only at 100 min in group BI; vitamin E consumption was significantly higher only in groups BII and BIII. When groups were compared by intensity at each swimming time there were no differences between I, II, and III at 50 min for any of the substances analyzed (MDA, GSH, and vitamin E), but at 100 min opposite effects were observed for GSH and vitamin E, with vitamin E consumption and GSH recovery occurring with increasing weight load. Higher concentrations of skeletal muscle MDA could indicate elevated lipid peroxidation at each time and exercise intensity, with highest MDA levels observed after the longest exercise duration and at the highest intensity. The layer-line mode of utilization of body antioxidants could explain the concentrations of GSH and vitamin E: first the use of GSH, even with minor oxidative stress, and then vitamin E consumption only in the presence of greater and more prolonged oxidative stress, indicating the necessity of adequate body levels of both antioxidants for proper utilization by the body antioxidant defense system.


2016 ◽  
Vol 48 ◽  
pp. 578-579
Author(s):  
Vitor R. Muñoz ◽  
Inês S. Lima ◽  
Leandro P. Moura ◽  
Rafael C. Gaspar ◽  
Rania A. Mekary ◽  
...  

Oncotarget ◽  
2017 ◽  
Vol 8 (12) ◽  
pp. 20428-20440 ◽  
Author(s):  
Mariana Janini Gomes ◽  
Paula Felippe Martinez ◽  
Luana Urbano Pagan ◽  
Ricardo Luiz Damatto ◽  
Marcelo Diacardia Mariano Cezar ◽  
...  

Life Sciences ◽  
2020 ◽  
Vol 252 ◽  
pp. 117630 ◽  
Author(s):  
Anand Thirupathi ◽  
Ricardo A. Pinho ◽  
Yan-Zhong Chang

2018 ◽  
Vol 2018 ◽  
pp. 1-15 ◽  
Author(s):  
C. Andreani ◽  
C. Bartolacci ◽  
M. Guescini ◽  
M. Battistelli ◽  
V. Stocchi ◽  
...  

Aging skeletal muscles are characterized by a progressive decline in muscle mass and muscular strength. Such muscular dysfunctions are usually associated with structural and functional alterations of skeletal muscle mitochondria. The senescence-accelerated mouse-prone 8 (SAMP8) model, characterized by premature aging and high degree of oxidative stress, was used to investigate whether a combined intervention with mild physical exercise and ubiquinol supplementation was able to improve mitochondrial function and preserve skeletal muscle health during aging. 5-month-old SAMP8 mice, in a presarcopenia phase, have been randomly divided into 4 groups (n=10): untreated controls and mice treated for two months with either physical exercise (0.5 km/h, on a 5% inclination, for 30 min, 5/7 days per week), ubiquinol 10 (500 mg/kg/day), or a combination of exercise and ubiquinol. Two months of physical exercise significantly increased mitochondrial damage in the muscles of exercised mice when compared to controls. On the contrary, ubiquinol and physical exercise combination significantly improved the overall status of the skeletal muscle, preserving mitochondrial ultrastructure and limiting mitochondrial depolarization induced by physical exercise alone. Accordingly, combination treatment while promoting mitochondrial biogenesis lowered autophagy and caspase 3-dependent apoptosis. In conclusion, the present study shows that ubiquinol supplementation counteracts the deleterious effects of physical exercise-derived ROS improving mitochondrial functionality in an oxidative stress model, such as SAMP8 in the presarcopenia phase.


Antioxidants ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 323
Author(s):  
Maravillas Sánchez Macarro ◽  
Vicente Ávila-Gandía ◽  
Silvia Pérez-Piñero ◽  
Fernando Cánovas ◽  
Ana María García-Muñoz ◽  
...  

This randomized double-blind and controlled single-center clinical trial was designed to evaluate the effect of a 6-week intake of a probiotic product (1 capsule/day) vs. a placebo on an oxidative stress model of physical exercise (high intensity and duration) in male cyclists (probiotic group, n = 22; placebo, n = 21). This probiotic included three lyophilized strains (Bifidobacterium longum CECT 7347, Lactobacillus casei CECT 9104, and Lactobacillus rhamnosus CECT 8361). Study variables were urinary isoprostane, serum malondialdehyde (MDA), serum oxidized low-density lipoprotein (Ox-LDL), urinary 8-hydroxy-2′-deoxiguanosine (8-OHdG), serum protein carbonyl, serum glutathione peroxidase (GPx), and serum superoxide dismutase (SOD). At 6 weeks, as compared with baseline, significant differences in 8-OHdG (Δ mean difference −10.9 (95% CI −14.5 to −7.3); p < 0.001), MDA (Δ mean difference −207.6 (95% CI −349.1 to −66.1; p < 0.05), and Ox-LDL (Δ mean difference −122.5 (95% CI −240 to −4.5); p < 0.05) were found in the probiotic group only. Serum GPx did not increase in the probiotic group, whereas the mean difference was significant in the placebo group (477.8 (95% CI 112.5 to 843.2); p < 0.05). These findings suggest an antioxidant effect of this probiotic on underlying interacting oxidative stress mechanisms and their modulation in healthy subjects. The study was registered in ClinicalTrials.gov (NCT03798821).


PLoS ONE ◽  
2017 ◽  
Vol 12 (6) ◽  
pp. e0178900 ◽  
Author(s):  
Francesca Accattato ◽  
Marta Greco ◽  
Salvatore A. Pullano ◽  
Ilaria Carè ◽  
Antonino S. Fiorillo ◽  
...  

Redox Biology ◽  
2018 ◽  
Vol 17 ◽  
pp. 315-322 ◽  
Author(s):  
Agnès Martin ◽  
Camille Faes ◽  
Tadej Debevec ◽  
Chantal Rytz ◽  
Grégoire Millet ◽  
...  

Author(s):  
Luiza Souza Marques ◽  
Vanessa Angonesi Zborowski ◽  
Suelen Osório Heck ◽  
Bruna da Cruz Weber Fulco ◽  
Cristina Wayne Nogueira

Streptozotocin (STZ) is a substance used experimentally to induce a diabetes model, a metabolic disease associated with oxidative tissue damage. This study evaluated if dichloro-diphenyl diselenide (p-ClPhSe)2 modulates oxidative stress in peripheral tissues of diabetic mice. Male Swiss mice received a single STZ injection (i.p) at a dose of 200 mg/kg or its vehicle and were treated with (p-ClPhSe)2 (7 days, 5 mg/kg) or metformin (200 mg/kg, 2x/day). After, the mice were euthanized to collect liver, kidney, and skeletal muscle samples. In the liver, (p-ClPhSe)2 reduced TBARS and protein carbonyl levels and normalized the SOD activity in STZ-treated mice. In the kidney, (p-ClPhSe)2 reversed the increase in the reactive species levels but not the CAT activity reduction in STZ-treated mice. There was no evidence of oxidative damage in the skeletal muscle of STZ-treated mice, but an increase in the CAT activity and a reduction in non-protein thiol levels were found. (p-ClPhSe)2 did not reverse a decrease in hepatic and renal δ-aminolevulinic acid dehydratase activity in STZ-treated mice. The results show that the liver and kidney of STZ-treated mice were more susceptible to oxidative stress. This study reveals that (p-ClPhSe)2 modulated oxidative stress, which differently affected peripheral tissues of diabetic mice.


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