scholarly journals Swimming Prevents Memory Impairment by Increasing the Antioxidant Defense in an Animal Model of Duchenne Muscular Dystrophy

2019 ◽  
Author(s):  
Priscila Mantovani Nocetti Ribeiro ◽  
Adriano Alberti ◽  
Viviane Freiberger ◽  
Letícia Ventura ◽  
Leoberto Ricardo Grigollo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Animal Model ◽  
Duchenne Muscular Dystrophy ◽  
Muscular Dystrophy ◽  
Antioxidant Defense ◽  
Antioxidant Defenses ◽  
Mdx Mice ◽  
Encephalic Structures ◽  
And Oxidative Stress

Duchenne muscular dystrophy (DMD) is a genetic disease which is associated to a progressive skeletical muscle degeneration. Swimming is usually indicated for avoiding impact and facilitating adherence because of a better adaptation to a warm water invironment and also for its benefits on cognition, and modulating memory and learning processes and for increasing antioxidant defenses in oxidative stress. The objective of this study was to evaluate the effects of a swimming protocol on memory and oxidative stress in an animal model of Duchenne muscular dystrophy. Methods: male mdx and wild type mice within 28 days were used in this study. The animals were trained in an stepped swimming protocol for four consecutive weeks. Twenty four hours after the last exercise day, aversive memory and habituation memory tests were performed and removed the encephalic structures of striatus, pre frontal cortex, hippocampus, and cortex and gastrocnemius and diafragma muscles to evaluate protein carbonilation and lipid peroxidation and free thiols. Results: it was verified that swimming was able to reduce significantly the levels of lipid peroxidation and protein carbonilation in gastrocnemius and hippocampus and striatus in exercised animals. Swimming has also prevented lipid peroxidation in diafragma. Besides, this swimming protocol was able to increase free thiols in gastrocnemius, diafragma and in analysed SNC structures. These results showed that swimming prevented aversive and habituation memory in mdx mice.

scholarly journals Swimming improves memory and antioxidant defense in an animal model of duchenne muscular dystrophy

2021 ◽  
Author(s):  
Priscila Mantovani Nocetti ◽  
Adriano Alberti ◽  
Viviane Freiberger ◽  
Letícia Ventura ◽  
Leoberto Ricardo Grigollo ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Animal Model ◽  
Duchenne Muscular Dystrophy ◽  
Muscular Dystrophy ◽  
Antioxidant Defense ◽  
Developmental Delays ◽  
Muscle Degeneration ◽  
Wild Type ◽  
And Oxidative Stress

Abstract Duchenne muscular dystrophy (DMD) is a genetic disease, which is associated to progressive skeletal muscle degeneration. In humans, DMD has early onset, causes developmental delays, and is a devastating disease that drastically diminishes the quality of life of the young individuals affected. The objective of this study was to evaluate the effects of a swimming protocol on memory and oxidative stress in an animal model of Duchenne muscular dystrophy. Male mdx and wild type mice within 28 days were used in this study. The animals were trained in a stepped swimming protocol for four consecutive weeks. It was verified that swimming was able to reduce significantly the levels of lipid peroxidation and protein carbonilation in gastrocnemius and hippocampus and striatum in exercised animals. Swimming has also prevented lipid peroxidation in diaphragm. Besides, this swimming protocol was able to increase free thiols in gastrocnemius, diaphragm and in all central nervous system structures. These results showed that a protocol of swimming as an aerobic exercise of low intensity, for four weeks, prevented aversive memory and habituation in mdx mice.

scholarly journals Swimming Improves Memory and Antioxidant Defense in an Animal Model of Duchenne Muscular Dystrophy

2021 ◽  
Author(s):  
Priscila Mantovani Nocetti ◽  
Adriano Alberti ◽  
Viviane Freiberger ◽  
Letícia Ventura ◽  
Leoberto Ricardo Grigollo ◽  
...  
Keyword(s):  
Animal Model ◽  
Duchenne Muscular Dystrophy ◽  
Muscular Dystrophy ◽  
Antioxidant Defense

scholarly journals Wheat Kernel Ingestion Protects from Progression of Muscle Weakness in mdx Mice, an Animal Model of Duchenne Muscular Dystrophy

1996 ◽  
Vol 40 (3) ◽  
pp. 444-449 ◽  
Author(s):  
Christoph Hübner ◽  
Hans-Anton Lehr ◽  
Robert Bodlaj ◽  
Barbara Finckh ◽  
Konrad Oexle ◽  
...  
Keyword(s):  
Animal Model ◽  
Duchenne Muscular Dystrophy ◽  
Muscular Dystrophy ◽  
Muscle Weakness ◽  
Mdx Mice ◽  
Wheat Kernel

scholarly journals Changes in Bone Metabolism and Antioxidant Defense Systems in Menopause-Induced Rats fed Bran Extract from Dark Purple Rice (Oryza sativa L. Cv. Superjami)

Nutrients ◽  
2021 ◽  
Vol 13 (9) ◽  
pp. 2926
Author(s):  
Soo Im Chung ◽  
Su Noh Ryu ◽  
Mi Young Kang
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Bone Loss ◽  
Bone Metabolism ◽  
Rice Bran ◽  
Antioxidant Defense ◽  
Control Group ◽  
Defense Systems ◽  
Antioxidant Defense Systems ◽  
And Oxidative Stress

Menopause is a matter of concern for women’s health due to a deficiency of female hormones; additionally, reactive oxygen species and aging can cause osteoporosis. Food becomes increasingly interesting as a menopausal woman’s alternative to hormone therapy. The effects of ethanol extracts from dark purple Superjami rice bran on bone metabolism and antioxidant defense systems in menopause-induced animal models were evaluated. Female rats underwent sham surgery or were ovariectomized to induce a menopause-like state. Rats were divided into a sham control group (SHAM), an ovariectomized control group (OVX), and an ovariectomized grou supplemented with Superjami rice bran extract group (OVX-S) and fed for 8 weeks. The OVX groups exhibited significantly more weight gain, amounts of bone turnover biochemical markers (alkaline phosphatase, osteocalcin, and C-terminal telopeptide), bone loss, lipid-peroxidation and oxidative stress than the SHAM group. However, Superjami bran extract added to the diet resulted in a significant reduction in body weight and lipid peroxidation, as well as enhanced bone metabolism and antioxidant enzyme activities, in ovariectomized rats. These results propound that extracts from Superjami rice bran have therapeutic potentiality against bone loss and oxidative stress in menopause-induced states and will be useful in preventing postmenopausal osteoporosis and oxidative damage.

MDX mouse myopathy I: Presence or absence of sarcolemmal lesions in tibialis anterior muscles from mice of different ages

1989 ◽  
Vol 47 ◽  
pp. 1070-1071
Author(s):  
H.D. Geissinger ◽  
L.D. Rhodes
Keyword(s):  
Animal Model ◽  
Duchenne Muscular Dystrophy ◽  
Muscular Dystrophy ◽  
Tibialis Anterior ◽  
Extensor Digitorum Longus ◽  
Morphological Analysis ◽  
Control Mouse ◽  
Mdx Mouse ◽  
Mdx Mice ◽  
Recent Interest

Since the ‘mdx’ mouse appears to have the same basic defect as sufferers of human Duchenne Muscular Dystrophy (DMD), much recent interest in this possible animal model for the human disease has been generated. Perforations in the sarcolemma have been reported recently in the necrotic tibialis anterior (TA) of 35-days-old and the extensor digitorum longus muscles of 39-days-old ‘mdx’ mice. It is the purpose of this communication to find out if these lesions occur not only in necrotic, but also in unaffected, or in centronucleated fibers of the TA of mice which are younger than 35, or older than 39 days.METHODS: TA from 22-, 25-, 41-, 61- and 99-days-old C57BL/10ScSn/MDX and C57BL/lOScSn control mice were pinned on corkboard in a relaxed state, prefixed for 30 minutes in 2.5% glutaraldehyde followed by routine processing for TEM. Appropriate micrographs were evaluated for a more detailed morphological analysis of the sarcolemma (SL) and the basal lamina (BL).RESULTS: It should be stated beforehand that in all muscles examined the BL appeared to be intact. In the muscles of a 25-days-old control mouse the SL appeared quite intact (FIG. 1). In contrast to this small perforations or large tears in the SL could be seen in otherwise unaffected muscles of 22- (FIG. 2), 25- and 41-days-old ‘mdx’ mice, as well as in necrotic and regenerating fibers of mice from these ages.

scholarly journals A Blood Biomarker for Duchenne Muscular Dystrophy Shows That Oxidation State of Albumin Correlates with Protein Oxidation and Damage in Mdx Muscle

Antioxidants ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1241
Author(s):  
Basma A. Al-Mshhdani ◽  
Miranda D. Grounds ◽  
Peter G. Arthur ◽  
Jessica R. Terrill
Keyword(s):  
Oxidative Stress ◽  
Duchenne Muscular Dystrophy ◽  
Muscular Dystrophy ◽  
Blood Protein ◽  
Mdx Mouse ◽  
Mdx Mice ◽  
Thiol Oxidation ◽  
Plasma Albumin ◽  
Blood Biomarker ◽  
Muscle Wasting Disease

Duchenne muscular dystrophy (DMD) is a severe X-linked muscle wasting disease with no cure. While the precise mechanisms of progressive dystropathology remain unclear, oxidative stress caused by excessive generation of oxidants is strongly implicated. Blood biomarkers that could track oxidant levels in tissues would be valuable to measure the effectiveness of clinical treatments for DMD; our research has focused on developing such biomarkers. One target of oxidants that has the potential to be harnessed as a clinical biomarker is the thiol side chain of cysteine 34 (Cys34) of the blood protein albumin. This study using the mdx mouse model of DMD shows that in plasma, albumin Cys34 undergoes thiol oxidation and these changes correlate with levels of protein thiol oxidation and damage of the dystrophic muscles. A comparison with the commonly used biomarker protein carbonylation, confirmed that albumin thiol oxidation is the more sensitive plasma biomarker of oxidative stress occurring in muscle tissue. We show that plasma albumin oxidation reflects muscle dystropathology, as increased after exercise and decreased after taurine treatment of mdx mice. These data support the use of albumin thiol oxidation as a blood biomarker of dystropathology to assist with advancing clinical development of therapies for DMD.

Effects ofSpirulina platensison lipid peroxidation, antioxidant defenses, and tissue damage in kidney of alloxan-induced diabetic rats

2018 ◽  
Vol 43 (4) ◽  
pp. 345-354 ◽  
Author(s):  
Manel Gargouri ◽  
Houda Hamed ◽  
Amel Akrouti ◽  
Xavier Dauvergne ◽  
Christian Magné ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Rat Kidney ◽  
Histological Study ◽  
Diabetic Rats ◽  
Antioxidant Defenses ◽  
Diabetic Rat ◽  
Antioxidant Enzyme Activities ◽  
Chronic Hyperglycemia ◽  
And Oxidative Stress

Chronic hyperglycemia in diabetes causes free radicals overproduction, which contributes to the development of diabetic nephropathy. In modern medicine, no satisfactory therapy is available to cure diabetes mellitus. In that context, we investigated the potential therapeutic action of spirulina-enriched diet on renal impairment and oxidative stress in diabetic rats. Diabetes was induced by a single subcutaneous injection of alloxan (120 mg·kg−1) in rats. Following alloxan treatment, male Wistar rats were fed daily with 5% spirulina-enriched diet or treated with insulin (0.5 IU·rat−1) for 3 weeks. Diabetes was associated with hyperglycemia, increase in renal oxidative parameters (lipid peroxidation, thiobarbituric-acid reactive substances, protein carbonyl and advanced oxidation protein products levels, changes in antioxidant enzyme activities), and nephropathology markers. The renal injury induced by alloxan was confirmed by histological study of the diabetic rat kidney. Treatment with spirulina or insulin significantly ameliorated renal dysfunction by reducing oxidative stress, while rats recovered normal kidney histology. Overall, this study indicates that spirulina is efficient in inhibiting hyperglycemia and oxidative stress induced by diabetes, and suggests that the administration of this alga may be helpful in the prevention of diabetic complications. This amelioration was even more pronounced than that caused by insulin injection.

scholarly journals SR Ca2+ handling in unbranched, immediately post-necrotic fast-twitch mdx fibres is similar to wt littermates

2021 ◽  
Author(s):  
Stephen Chan ◽  
Sindy L.L. Kueh ◽  
John W Morley ◽  
Stewart Head
Keyword(s):  
Animal Model ◽  
Duchenne Muscular Dystrophy ◽  
Muscular Dystrophy ◽  
Rise Time ◽  
Mdx Mice ◽  
Regenerative Processes ◽  
Dystrophin Deficiency ◽  
Massive Necrosis ◽  
Early Effects ◽  
Fast Twitch

There is a lack of consensus in the literature regarding the effects of dystrophin deficiency on the Ca2+ handling properties of the sarcoplasmic reticulum (SR) in mdx mice, an animal model of Duchenne muscular dystrophy. One possible reason for this is that only a few studies control for the presence of branched fibres. Fibre branching, a consequence of degenerative-regenerative processes such as muscular dystrophy, has in itself a significant influence on the function of the SR. In our present study we attempt to detect early effects of dystrophin deficiency on SR Ca2+ handling by using unbranched fibres from the immediate post-necrotic stage in mdx mice (just regenerated following massive necrosis). Using kinetically-corrected Fura-2 fluorescence signals measured during twitch and tetanus, we analysed the amplitude, rise time and decay time of Δ[Ca2+]i in unfatigued and fatigued fibres. Decay was also resolved into SR pump and SR leak components. Fibres from mdx mice were similar in all respects to fibres from wt littermates apart from: (i) a longer rise time and slower rate of rise of [Ca2+]i during a tetanus; and (ii) a mitigation of the fall in Δ[Ca2+]i amplitude during the course of fatigue. Our findings suggest that the early effects of a loss of dystrophin on SR Ca2+ handling are only slight, and differ from the widely held view that there is significant Ca2+ pathology in mdx mice. It may be that Ca2+pathology is magnified by progressive branching and degeneration.

ELECTROMYOGRAPHIC (EMG) CHARACTERIZATION OF THE MDX MICE: AN ANIMAL MODEL FOR DUCHENNE MUSCULAR DYSTROPHY

2005 ◽  
Vol 84 (3) ◽  
pp. 202 ◽  
Author(s):  
Jay J. Han ◽  
Jennifer J. Ra ◽  
Richard T. Abresch ◽  
Lawrence R. Robinson ◽  
Jeffrey S. Chamberlain ◽  
...  
Keyword(s):  
Animal Model ◽  
Duchenne Muscular Dystrophy ◽  
Muscular Dystrophy ◽  
Mdx Mice
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