Effects of duration of thermal stress on growth performance, serum oxidative stress indices, the expression and localization of ABCG2 and mitochondria ROS production of skeletal muscle, small intestine and immune organs in broilers

2019 ◽  
Vol 85 ◽  
pp. 102420 ◽  
Author(s):  
Juhua Wang ◽  
Xiuheng Xue ◽  
Qi Liu ◽  
Suzi Zhang ◽  
Mengling Peng ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Small Intestine ◽  
Thermal Stress ◽  
Growth Performance ◽  
Ros Production ◽  
Stress Indices ◽  
Immune Organs

scholarly journals Mitochondrial-targeted antioxidants protect skeletal muscle against immobilization-induced muscle atrophy

2011 ◽  
Vol 111 (5) ◽  
pp. 1459-1466 ◽  
Author(s):  
Kisuk Min ◽  
Ashley J. Smuder ◽  
Oh-sung Kwon ◽  
Andreas N. Kavazis ◽  
Hazel H. Szeto ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Muscle Atrophy ◽  
Muscle Fibers ◽  
Skeletal Muscle Atrophy ◽  
Ros Production ◽  
Oxygen Species ◽  
Mitochondrial Ros ◽  
Protease Activation ◽  
Limb Immobilization

Prolonged periods of muscular inactivity (e.g., limb immobilization) result in skeletal muscle atrophy. Although it is established that reactive oxygen species (ROS) play a role in inactivity-induced skeletal muscle atrophy, the cellular pathway(s) responsible for inactivity-induced ROS production remain(s) unclear. To investigate this important issue, we tested the hypothesis that elevated mitochondrial ROS production contributes to immobilization-induced increases in oxidative stress, protease activation, and myofiber atrophy in skeletal muscle. Cause-and-effect was determined by administration of a novel mitochondrial-targeted antioxidant (SS-31) to prevent immobilization-induced mitochondrial ROS production in skeletal muscle fibers. Compared with ambulatory controls, 14 days of muscle immobilization resulted in significant muscle atrophy, along with increased mitochondrial ROS production, muscle oxidative damage, and protease activation. Importantly, treatment with a mitochondrial-targeted antioxidant attenuated the inactivity-induced increase in mitochondrial ROS production and prevented oxidative stress, protease activation, and myofiber atrophy. These results support the hypothesis that redox disturbances contribute to immobilization-induced skeletal muscle atrophy and that mitochondria are an important source of ROS production in muscle fibers during prolonged periods of inactivity.

Activation of aconitase in mouse fast-twitch skeletal muscle during contraction-mediated oxidative stress

2007 ◽  
Vol 293 (3) ◽  
pp. C1154-C1159 ◽  
Author(s):  
Shi-Jin Zhang ◽  
Marie E. Sandström ◽  
Johanna T. Lanner ◽  
Anders Thorell ◽  
Håkan Westerblad ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Tricarboxylic Acid Cycle ◽  
Thigh Muscle ◽  
Ros Production ◽  
Atp Production ◽  
Aconitase Activity ◽  
Oxidation Reduction ◽  
Edl Muscle ◽  
Fast Twitch

Aconitase is a mitochondrial enzyme that converts citrate to isocitrate in the tricarboxylic acid cycle and is inactivated by reactive oxygen species (ROS). We investigated the effect of exercise/contraction, which is associated with elevated ROS production, on aconitase activity in skeletal muscle. Humans cycled at 75% of maximal workload, followed by six 60-s bouts at 125% of maximum workload. Biopsies were taken from the thigh muscle at rest and after the submaximal and supramaximal workloads. Isolated mouse extensor digitorum longus (EDL; fast twitch) and soleus (slow twitch) muscles were stimulated to perform repeated contractions for 10 min. Muscles were analyzed for enzyme activities and glutathione status. Exercise did not affect aconitase activity in human muscle despite increased oxidative stress, as judged by elevated levels of oxidized glutathione. Similarly, repeated contractions did not alter aconitase activity in soleus muscle. In contrast, repeated contractions significantly increased aconitase activity in EDL muscle by ∼50%, despite increased ROS production. This increase was not associated with a change in the amount of immunoreactive aconitase (Western blot) but was markedly inhibited by cyclosporin A, an inhibitor of the protein phosphatase calcineurin. Immunoprecipitation experiments demonstrated that aconitase was phosphorylated on serine residues. Aconitase in cell-free extracts was inactivated by the addition of the ROS hydrogen peroxide. In conclusion, the results suggest that aconitase activity can be regulated by at least two mechanisms: oxidation/reduction and phosphorylation/dephosphorylation. During contraction, a ROS-mediated inactivation of aconitase can be overcome, possibly by dephosphorylation of the enzyme. The dual-control system may be important in maintaining aerobic ATP production during muscle contraction.

Stanozolol treatment decreases the mitochondrial ROS generation and oxidative stress induced by acute exercise in rat skeletal muscle

2011 ◽  
Vol 110 (3) ◽  
pp. 661-669 ◽  
Author(s):  
Ana Saborido ◽  
Alba Naudí ◽  
Manuel Portero-Otín ◽  
Reinald Pamplona ◽  
Alicia Megías
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Fatty Acid Composition ◽  
Mitochondrial Membrane ◽  
Acute Exercise ◽  
Ros Generation ◽  
Ros Production ◽  
Rat Skeletal Muscle ◽  
Mitochondrial Ros ◽  
Exercise Induced

Anabolic androgenic steroids are used in the sport context to enhance muscle mass and strength and to increase muscle fatigue resistance. Since muscle fatigue has been related to oxidative stress caused by an exercise-linked reactive oxygen species (ROS) production, we investigated the potential effects of a treatment with the anabolic androgenic steroid stanozolol against oxidative damage induced on rat skeletal muscle mitochondria by an acute bout of exhaustive exercise. Mitochondrial ROS generation with complex I- and complex II-linked substrates was increased in exercised control rats, whereas it remained unchanged in the steroid-treated animals. Stanozolol treatment markedly reduced the extent of exercise-induced oxidative damage to mitochondrial proteins, as indicated by the lower levels of the specific markers of protein oxidation, glycoxidation, and lipoxidation, and the preservation of the activity of the superoxide-sensitive enzyme aconitase. This effect was not due to an enhancement of antioxidant enzyme activities. Acute exercise provoked changes in mitochondrial membrane fatty acid composition characterized by an increased content in docosahexaenoic acid. In contrast, the postexercise mitochondrial fatty acid composition was not altered in stanozolol-treated rats. Our results suggest that stanozolol protects against acute exercise-induced oxidative stress by reducing mitochondrial ROS production, in association with a preservation of mitochondrial membrane properties.

scholarly journals Oxidative Metabolism Genes Are Not Responsive to Oxidative Stress in Rodent Beta Cell Lines

2012 ◽  
Vol 2012 ◽  
pp. 1-5 ◽  
Author(s):  
Faer Morrison ◽  
Karen Johnstone ◽  
Anna Murray ◽  
Jonathan Locke ◽  
Lorna W. Harries
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Beta Cell ◽  
Beta Cells ◽  
Oxidative Metabolism ◽  
Pancreatic Beta Cells ◽  
Ros Production ◽  
Altered Expression ◽  
Beta Cell Line

Altered expression of oxidative metabolism genes has been described in the skeletal muscle of individuals with type 2 diabetes. Pancreatic beta cells contain low levels of antioxidant enzymes and are particularly susceptible to oxidative stress. In this study, we explored the effect of hyperglycemia-induced oxidative stress on a panel of oxidative metabolism genes in a rodent beta cell line. We exposed INS-1 rodent beta cells to low (5.6 mmol/L), ambient (11 mmol/L), and high (28 mmol/L) glucose conditions for 48 hours. Increases in oxidative stress were measured using the fluorescent probe dihydrorhodamine 123. We then measured the expression levels of a panel of 90 oxidative metabolism genes by real-time PCR. Elevated reactive oxygen species (ROS) production was evident in INS-1 cells after 48 hours (P<0.05). TLDA analysis revealed a significant (P<0.05) upregulation of 16 of the 90 genes under hyperglycemic conditions, although these expression differences did not reflect differences in ROS. We conclude that although altered glycemia may influence the expression of some oxidative metabolism genes, this effect is probably not mediated by increased ROS production. The alterations to the expression of oxidative metabolism genes previously observed in human diabetic skeletal muscle do not appear to be mirrored in rodent pancreatic beta cells.

scholarly journals The effect of cassia seed extract on the regulation of the LKB1–AMPK–GLUT4 signaling pathway in the skeletal muscle of diabetic rats to improve the insulin sensitivity of the skeletal muscle

2019 ◽  
Vol 11 (1) ◽  
Author(s):  
Qiu-Ying Wang ◽  
Ai-Hua Tong ◽  
Ying-Ying Pan ◽  
Xian-Dang Zhang ◽  
Wen-Yu Ding ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Blood Glucose ◽  
Lipid Level ◽  
Blood Lipid ◽  
Seed Extract ◽  
Blood Lipid Level ◽  
Stress Indices ◽  
Insulin Tolerance ◽  
And Oxidative Stress

Abstract Background This study aimed to observe the hypoglycemic effect of cassia seed extract in rats with type-2 diabetes mellitus and its effect on reducing insulin resistance in the skeletal muscle. Methods 50 rats were randomly divided into the normal, model, high-dose, middle-dose, and low-dose groups of cassia seed extract (n = 10 each). A high-fat diet combined with streptozotocin administration was adopted to build type 2 diabetes models. The cassia seed extract groups were fed different concentrations cassia seed extract while the normal and model groups were fed the same volume of normal saline. The weight, FINS, GIR, insulin tolerance, blood glucose and blood lipid level, oxidative stress indices and expressions related to the LKB1–AMPK–GLUT4 pathway were detected and compared between the two groups. Results Compared with the normal group, the model group showed lower weight, glucose infusion rate and expressions related to LKB1–AMPK–GLUT4 pathway and higher FINS, insulin tolerance, blood glucose and blood lipid level and oxidative stress indices (all P < 0.05). Compared with the model group, higher weight, glucose infusion rate and expressions related to LKB1–AMPK–GLUT4 pathway and lower FINS, insulin tolerance, blood glucose and blood lipid level and oxidative stress indices were observed in all groups that were administered cassia see extract (all P < 0.05). Conclusion Cassia seed extract could noticeably improve the insulin resistance of diabetic rats and enhance the insulin sensitivity of their skeletal muscles. Its mechanism may be related to damage repair of the LKB1–AMPK–GLUT4 signaling pathway and oxidative stress in the skeletal muscle.

Growth performance, oxidative stress indices and hepatic carbohydrate metabolic enzymes activities of juvenile Nile tilapia,Oreochromis niloticusL., in response to dietary starch to protein ratios

2013 ◽  
Vol 46 (1) ◽  
pp. 14-27 ◽  
Author(s):  
Mohamed Salah Azaza ◽  
Noura Khiari ◽  
Mohamed Naceur Dhraief ◽  
Néji Aloui ◽  
Mohamed Mejdeddine Kraϊem ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Growth Performance ◽  
Nile Tilapia ◽  
Metabolic Enzymes ◽  
Stress Indices ◽  
Enzymes Activities ◽  
Dietary Starch

scholarly journals Inhibition of xanthine oxidase reduces hyperglycemia-induced oxidative stress and improves mitochondrial alterations in skeletal muscle of diabetic mice

2011 ◽  
Vol 300 (3) ◽  
pp. E581-E591 ◽  
Author(s):  
Amélie Bravard ◽  
Charlotte Bonnard ◽  
Annie Durand ◽  
Marie-Agnès Chauvin ◽  
Roland Favier ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Xanthine Oxidase ◽  
Ros Production ◽  
Diabetic Mice ◽  
Protein Levels ◽  
Mitochondrial Alterations ◽  
High Sucrose Diet ◽  
High Sucrose

Reactive oxygen species (ROS) have been widely implicated in the pathogenesis of diabetes and more recently in mitochondrial alterations in skeletal muscle of diabetic mice. However, so far the exact sources of ROS in skeletal muscle have remained elusive. Aiming at better understanding the causes of mitochondrial alterations in diabetic muscle, we designed this study to characterize the sites of ROS production in skeletal muscle of streptozotocin (STZ)-induced diabetic mice. Hyperglycemic STZ mice showed increased markers of systemic and muscular oxidative stress, as evidenced by increased circulating H2O2 and muscle carbonylated protein levels. Interestingly, insulin treatment reduced hyperglycemia and improved systemic and muscular oxidative stress in STZ mice. We demonstrated that increased oxidative stress in muscle of STZ mice is associated with an increase of xanthine oxidase (XO) expression and activity and is mediated by an induction of H2O2 production by both mitochondria and XO. Finally, treatment of STZ mice, as well as high-fat and high-sucrose diet-fed mice, with oxypurinol reduced markers of systemic and muscular oxidative stress and prevented structural and functional mitochondrial alterations, confirming the in vivo relevance of XO in ROS production in diabetic mice. These data indicate that mitochondria and XO are the major sources of hyperglycemia-induced ROS production in skeletal muscle and that the inhibition of XO reduces oxidative stress and improves mitochondrial alterations in diabetic muscle.

Melatonin: a novel strategy for prevention of obesity and fat accumulation in peripheral organs through the improvements of circadian rhythms and antioxidative capacity

2020 ◽  
Vol 3 (1) ◽  
pp. 58-76 ◽  
Author(s):  
Bohan Rong ◽  
Qiong Wu ◽  
Chao Sun
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Circadian Rhythms ◽  
Regulatory Mechanisms ◽  
Antioxidative Capacity ◽  
Unicellular Alga ◽  
Peripheral Tissues ◽  
Peripheral Organs ◽  
Regulatory Effects ◽  
Novel Strategy

Melatonin is a well-known molecule for its involvement in circadian rhythm regulation and its contribution to protection against oxidative stress in organisms including unicellular alga, animals and plants. Currently, the bio-regulatory effects of melatonin on the physiology of various peripheral tissues have drawn a great attention of scientists. Although melatonin was previously defined as a neurohormone secreted from pineal gland, recently it has been identified that virtually, every cell has the capacity to synthesize melatonin and the locally generated melatonin has multiple pathophysiological functions, including regulations of obesity and metabolic syndromes. Herein, we focus on the effects of melatonin on fat deposition in various peripheral organs/tissues. The two important regulatory mechanisms related to the topic, i.e., the improvements of circadian rhythms and antioxidative capacity will be thoroughly discussed since they are linked to several biomarkers involved in obesity and energy imbalance, including metabolism and immunity. Furthermore, several other functions of melatonin which may serve to prevent or promote obesity and energy dysmetabolism-induced pathological states are also addressed. The organs of special interest include liver, pancreas, skeletal muscle, adipose tissue and the gut microbiota.

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