scholarly journals Diazoxide and Exercise Enhance Muscle Contraction during Obesity by Decreasing ROS Levels, Lipid Peroxidation, and Improving Glutathione Redox Status

Antioxidants ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 1232
Author(s):  
Mariana Gómez-Barroso ◽  
Koré M. Moreno-Calderón ◽  
Elizabeth Sánchez-Duarte ◽  
Christian Cortés-Rojo ◽  
Alfredo Saavedra-Molina ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Lipid Peroxidation ◽  
Muscle Contraction ◽  
Katp Channel ◽  
Metabolic Stress ◽  
Muscular Contraction ◽  
Redox Status ◽  
Glutathione Redox ◽  
Katp Channel Openers

Obesity causes insulin resistance and hyperinsulinemia which causes skeletal muscle dysfunction resulting in a decrease in contraction force and a reduced capacity to avoid fatigue, which overall, causes an increase in oxidative stress. KATP channel openers such as diazoxide and the implementation of exercise protocols have been reported to be actively involved in protecting skeletal muscle against metabolic stress; however, the effects of diazoxide and exercise on muscle contraction and oxidative stress during obesity have not been explored. This study aimed to determine the effect of diazoxide in the contraction of skeletal muscle of obese male Wistar rats (35 mg/kg), and with an exercise protocol (five weeks) and the combination from both. Results showed that the treatment with diazoxide and exercise improved muscular contraction, showing an increase in maximum tension and total tension due to decreased ROS and lipid peroxidation levels and improved glutathione redox state. Therefore, these results suggest that diazoxide and exercise improve muscle function during obesity, possibly through its effects as KATP channel openers.

scholarly journals Effects of cisplatin on lipid peroxidation and the glutathione redox status in the liver of male rats: The protective role of selenium

2010 ◽  
Vol 62 (1) ◽  
pp. 75-82 ◽  
Author(s):  
Ivana Trbojevic ◽  
Branka Ognjanovic ◽  
Natasa Djordjevic ◽  
Snezana Markovic ◽  
A.S. Stajn ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Membrane Lipids ◽  
Redox Status ◽  
Protective Role ◽  
Male Rats ◽  
Albino Rats ◽  
Wistar Albino Rats ◽  
Glutathione Redox

The role of oxidative stress in cisplatin (CP) toxicity and its prevention by pretreatment with selenium (Se) was investigated. Male Wistar albino rats were injected with a single dose of cisplatin (7.5 mg CP/kg b.m., i.p.) and selenium (6 mg Se/kg b.m, as Na2SeO3, i.p.) alone or in combination. The results suggest that CP intoxication induces oxidative stress and alters the glutathione redox status: reduced glutathione (GSH), oxidized glutathione (GSSG) and the GSH/GSSG ratio (GSH RI), resulting in increased lipid peroxidation (LPO) in rat liver. The pretreatment with selenium prior to CP treatment showed a protective effect against the toxic influence of CP on peroxidation of the membrane lipids and an altering of the glutathione redox status in the liver of rats. From our results we conclude that selenium functions as a potent antioxidant and suggest that it can control CP-induced hepatotoxicity in rats.

scholarly journals Redox Status in Women with Rheumathoid Arthritis

2018 ◽  
Vol 0 (0) ◽  
Author(s):  
Aleksandra Vranic ◽  
Aleksandra Antovic ◽  
Nevena Draginic ◽  
Marijana Andjic ◽  
Marko Ravic ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Lipid Peroxidation ◽  
Superoxide Dismutase ◽  
Cartilage Damage ◽  
Thiobarbituric Acid ◽  
Antioxidant Defense System ◽  
Redox Status ◽  
Female Population

Abstract The aim of this study was to assess oxidative status and to set baseline characteristics for female population with established rheumatoid arthritis. Total of 42 patients with rheumatoid arthritis and 48 age- and sex-matched controls were included in the study. Clinical examination was performed and assessed disease activity. Peripheral blood samples were used for all the assays. The markers of oxidative stress were assessed, including plasma levels of index of lipid peroxidation - thiobarbituric acid reactive substances, hydrogen peroxide, superoxide anion radical, nitrites and activity of superoxide dismutase, catalase and reduced glutathione levels as antioxidant parameters. In the patients group, levels of hydrogen peroxide and index of lipid peroxidation were higher than in controls. Patients with rheumatoid arthritis had decreased superoxide dismutase and catalase activity compared to healthy subjects. Interestingly, controls had higher levels of nitrites compared to patients. Patients showed a marked increase in reactive oxygen species formation and lipid peroxidation as well as decrease in the activity of antioxidant defense system leading to oxidative stress which may contribute to tissue and cartilage damage and hence to the chronicity of the disease.

scholarly journals Effects of emphysema and training on glutathione oxidation in the hamster diaphragm

2000 ◽  
Vol 88 (6) ◽  
pp. 2054-2061 ◽  
Author(s):  
Leo M. A. Heunks ◽  
Aalt Bast ◽  
Cees L. A. van Herwaarden ◽  
Guido R. M. M. Haenen ◽  
P. N. Richard Dekhuijzen
Keyword(s):  
Oxidative Stress ◽  
Inverse Correlation ◽  
Redox Status ◽  
Tetanic Force ◽  
Twitch Force ◽  
Glutathione Oxidation ◽  
And Training ◽  
Glutathione Redox ◽  
Maximal Tetanic Force

Loading of skeletal muscles is associated with increased generation of oxidants, which in turn may impair muscle contractility. We investigated whether the load on the hamster diaphragm imposed by pulmonary emphysema induces oxidative stress, as indicated by glutathione oxidation, and whether the degree of glutathione oxidation is correlated with contractility of the diaphragm. In addition, the effect of 12 wk of treadmill exercise training on contractility and glutathione content in the normal (NH) and emphysematous hamster (EH) diaphragm was investigated. Training started 6 mo after elastase instillation. After the training period, glutathione content and in vitro contractility of the diaphragm were determined. Twitch force and maximal tetanic force were significantly reduced (by ∼30 and ∼15%, respectively) in EH compared with NH. In sedentary hamsters, the GSSG-to-GSH ratio was significantly elevated in the EH compared with the NH diaphragm. A significant inverse correlation was found between GSSG-to-GSH ratio and twitch force in the diaphragm ( P < 0.01). Training improved maximal tetanic force and reduced fatigability of the EH diaphragm but did not alter its glutathione content. In conclusion, 1) emphysema induces oxidative stress in the diaphragm, 2) training improves the contractile properties of the EH diaphragm, and 3) this improvement is not accompanied by changes in glutathione redox status.

153 ALLEVIATIVE EFFECTS OF ANTIOXIDANT ADMINISTRATION ON MATERNAL HYPERTHERMIA-INDUCED EARLY EMBRYONIC DEATH IN MICE

2006 ◽  
Vol 18 (2) ◽  
pp. 184
Author(s):  
T. Matsuzuka ◽  
N. Sakamoto ◽  
M. Ozawa ◽  
A. Ushitani ◽  
M. Hirabayashi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Body Weight ◽  
Vitamin E ◽  
Radical Scavenging Activity ◽  
Radical Scavenging ◽  
Redox Status ◽  
Maternal Body ◽  
Early Embryos ◽  
Embryonic Death

Hyperthermia-induced early embryonic death is generally ascribed to the high susceptibility of early embryos to elevated maternal body temperature. However, recent studies have indicated that the disruption of embryonic development by maternal hyperthermia has relevance to not only high temperature exposure to the embryo, but also hyperthermia-associated changes in the maternal body. Hyperthermia enhances physiological production of reactive oxygen species (ROS) systemically. Early embryos are susceptible to oxidative stress and it becomes easy to arrest their development when the oxidative stress is exposed. These findings led us to speculate that maternal hyperthermia-induced early embryonic death is caused by an increase in oxidative stress to the embryo. Vitamin E and melatonin are both well known to function as antioxidants in vivo when they are administered exogenously. In this study, we administered vitamin E or melatonin to heat-stressed pregnant mice, aiming to alleviate the hyperthermia-induced embryonic death. Female mice were heat-stressed (35�C with 60% relative humidity) for 12 h on the day of mating. In Experiment 1, vitamin E (1000 mg/kg body weight) was injected intraperitoneally just before stress treatment, or melatonin (3 mg/kg body weight) was injected subcutaneously for every 2 h during heat exposure. Then, zygotes were collected and in vitro developmental ability was assessed. In Experiment 2, intracellular glutathione (GSH) content in the zygote, ROS level and free radical scavenging activity (FRSA) in the oviduct, and lipid peroxidation level in the liver were measured to evaluate the effects of melatonin administration on physiological redox status. All data were analyzed using one-way ANOVA followed by Fisher's protected least-significant test. The percentage of embryos that developed to the morula or blastocyst stage was significantly (P < 0.01) increased by administration of either vitamin E (58.6%) or melatonin (47.9%) compared with that in heat-stressed mice that were administered placebos (14.8%). Intracellular GSH content in zygotes derived from melatonin-administered mice was not significantly different from that in unstressed mice (1.67 and 1.82 pmol/zygote, respectively), whereas in heat-stressed mice that were administered placebo, intracellular GSH content was significantly decreased (1.48 pmol/zygote, P < 0.05) compared to that in unstressed mice. There were no significant differences in lipid peroxidation levels in the liver and in ROS levels in the oviduct between melatonin-administered stressed mice and unstressed mice, although these parameters in heat-stressed mice with placebo were significantly higher than in unstressed mice (P < 0.05). Furthermore, FRSA in the oviduct was significantly (P < 0.05) higher in the melatonin-administered mice than in the heat-stressed mice. These findings suggest that antioxidant administration to heat-stressed mice alleviates the hyperthermia-induced early embryonic death, and this may be accomplished in part by maintaining a neutral redox status within the mother.

scholarly journals The Lipid Peroxidation By-Product 4-Hydroxy-2-Nonenal (4-HNE) Induces Insulin Resistance in Skeletal Muscle through Both Carbonyl and Oxidative Stress

Endocrinology ◽  
2012 ◽  
Vol 153 (5) ◽  
pp. 2099-2111 ◽  
Author(s):  
Nicolas J. Pillon ◽  
Marine L. Croze ◽  
Roxane E. Vella ◽  
Laurent Soulère ◽  
Michel Lagarde ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Lipid Peroxidation ◽  
And Oxidative Stress

scholarly journals Products of lipid peroxidation, but not membrane susceptibility to oxidative damage, are conserved in skeletal muscle following temperature acclimation

2015 ◽  
Vol 308 (5) ◽  
pp. R439-R448 ◽  
Author(s):  
Jeffrey M. Grim ◽  
Molly C. Semones ◽  
Donald E. Kuhn ◽  
Tamas Kriska ◽  
Agnes Keszler ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Lipid Peroxidation ◽  
Thermal Effects ◽  
Total Phospholipid ◽  
Acyl Chain ◽  
Morone Saxatilis ◽  
Redox Status ◽  
Temperature Acclimation ◽  
Effect Of Temperature ◽  
Phospholipid Content

Changes in oxidative capacities and phospholipid remodeling accompany temperature acclimation in ectothermic animals. Both responses may alter redox status and membrane susceptibility to lipid peroxidation (LPO). We tested the hypothesis that phospholipid remodeling is sufficient to offset temperature-driven rates of LPO and, thus, membrane susceptibility to LPO is conserved. We also predicted that the content of LPO products is maintained over a range of physiological temperatures. To assess LPO susceptibility, rates of LPO were quantified with the fluorescent probe C11-BODIPY in mitochondria and sarcoplasmic reticulum from oxidative and glycolytic muscle of striped bass ( Morone saxatilis) acclimated to 7°C and 25°C. We also measured phospholipid compositions, contents of LPO products [i.e., individual classes of phospholipid hydroperoxides (PLOOH)], and two membrane antioxidants. Despite phospholipid headgroup and acyl chain remodeling, these alterations do not counter the effect of temperature on LPO rates (i.e., LPO rates are generally not different among acclimation groups when normalized to phospholipid content and compared at a common temperature). Although absolute levels of PLOOH are higher in muscles from cold- than warm-acclimated fish, this difference is lost when PLOOH levels are normalized to total phospholipid. Contents of vitamin E and two homologs of ubiquinone are more than four times higher in mitochondria prepared from oxidative muscle of warm- than cold-acclimated fish. Collectively, our data demonstrate that although phospholipid remodeling does not provide a means for offsetting thermal effects on rates of LPO, differences in phospholipid quantity ensure a constant proportion of LPO products with temperature variation.

scholarly journals THE RATIO OF SYSTEMIC INFLAMMATION, OXIDATIVE STRESS AND GLUTATHIONE REDOX STATUS INDICATORS IN PATIENTS WITH CORONARY HEART DISEASE AND TYPE 2 DIABETES MELLITUS

2013 ◽  
Vol 19 (4) ◽  
pp. 356-366
Author(s):  
A. G. Moiseenok ◽  
I. V. Buko ◽  
I. V. Gorudko ◽  
E. E. Konstantinova ◽  
N. L. Tsapaeva ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Coronary Heart Disease ◽  
Redox Potential ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Redox Status ◽  
Glutathione Redox

Objective. To study and compare indicators of systemic inlammation and red blood cells glutathione redox potential by chronic oxidative stress (OS) in patients with coronary heart disease (CHD), type 2 diabetes mellitus (T2DM) and the combination of both diseases.Design and methods. The study included 35 patients with CHD and newly diagnosed T2DM, 109 patients with CHD, 19 patients with T2DM, and 89 healthy individuals. Systemic inlammation indicators were measured including concentration of interleukin (IL) 6 and 8, myeloperoxidase (MPO) and OS in plasma, oxidized (GSSG) and reduced (GSH) glutathione, as well as their ratio and redox potential (E), the activity of glutathione reductase (GR) and glutathione peroxidase (GP) in red blood cells.Results. Signiicant growth of systemic inlammation (IL-6, IL-8, MPO) indicators on the weakening antioxidant defense enzyme has been registered in patients with a combination of CHD and T2DM, a 3,4-fold reduction of GSH level, 5,8-fold of 2GSH/GSSH in red blood cells and E values towards the oxidized state at 36,3 mV were noted. These changes were less pronounced in CHD group and were absent in T2DM group. All subjects showed a decreased activity of GP and increased level of glycosylated hemoglobin. The correlation of E and activity GR have been found in patients with carbohydrate metabolism disorder. High positive relationship between IL concentration and red blood cells GR, E indicators has been identiied in patients with CHD and T2DM. There is a need to control and correct cellular redox potential in patients with CHD and T2DM.Conclusion. The combination of CHD and T2DM contributes to the decrease of red blood cells redox status glutathione secondary to the increased systemic inlammatory response and chronic OS indicators.

scholarly journals Evidence of Blood and Muscle Redox Status Imbalance in Experimentally Induced Renal Insufficiency in a Rabbit Model

2019 ◽  
Vol 2019 ◽  
pp. 1-14
Author(s):  
Konstantina P. Poulianiti ◽  
Aggeliki Karioti ◽  
Antonia Kaltsatou ◽  
Georgia I. Mitrou ◽  
Yiannis Koutedakis ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Renal Insufficiency ◽  
Redox Homeostasis ◽  
Rabbit Model ◽  
Thiobarbituric Acid ◽  
Redox Status ◽  
Protein Carbonyls ◽  
Blood Levels ◽  
End Stage

Chronic kidney disease (CKD) is accompanied by a disturbed redox homeostasis, especially in end-stage patients, which is associated with pathological complications such as anemia, atherosclerosis, and muscle atrophy. However, limited evidence exists about redox disturbances before the end stage of CKD. Moreover, the available redox literature has not yet provided clear associations between circulating and tissue-specific (muscle) oxidative stress levels. The aim of the study was to evaluate commonly used redox status indices in the blood and in two different types of skeletal muscle (psoas, soleus) in the predialysis stages of CKD, using an animal model of renal insufficiency, and to investigate whether blood redox status indices could be reflecting the skeletal muscle redox status. Indices evaluated included reduced glutathione (GSH), oxidized glutathione (GSSG), glutathione reductase (GR), catalase (CAT), total antioxidant capacity (TAC), protein carbonyls (PC), and thiobarbituric acid reactive substances (TBARS). Results showed that blood GSH was higher in the uremic group compared to the control (17.50±1.73 vs. 12.43±1.01, p=0.033). In both muscle types, PC levels were higher in the uremic group compared to the control (psoas: 1.086±0.294 vs. 0.596±0.372, soleus: 2.52±0.29 vs. 0.929±0.41, p<0.05). The soleus had higher levels of TBARS, PC, GSH, CAT, and GR and lower TAC compared to the psoas in both groups. No significant correlations in redox status indices between the blood and skeletal muscles were found. However, in the uremic group, significant correlations between the psoas and soleus muscles in PC, GSSG, and CAT levels emerged, not present in the control. Even in the early stages of CKD, a disturbance in redox homeostasis was observed, which seemed to be muscle type-specific, while blood levels of redox indices did not seem to reflect the intramuscular condition. The above results highlight the need for further research in order to identify the key mechanisms driving the onset and progression of oxidative stress and its detrimental effects on CKD patients.

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