Lipid peroxidation and superoxide dismutase activity in muscle and erythrocytes in Duchenne muscular dystrophy

Mechler, Ferenc; Imre, S.; Diószeghy, Péter

doi:10.1016/0022-510x(84)90150-3

Cited by 55 publications

(28 citation statements)

References 13 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Despite no signs of muscle pathology, investigators found increases in lipid peroxidation along with increases in the endogenous antioxidant enzymes. Similar findings (i.e., increased lipid peroxidation) have been recapitulated in studies of patients with DMD,152–159 suggesting that oxidative stress and damage contribute to the dystrophic process (Table 2).…”

Section: Increased Oxidative Stresssupporting

confidence: 78%

Exercise and duchenne muscular dystrophy: Toward evidence‐based exercise prescription

et al. 2011

View full text Add to dashboard Cite

To develop a rational framework for answering questions about the role of exercise in Duchenne muscular dystrophy (DMD), we focused on five pathophysiological mechanisms and offer brief hypotheses regarding how exercise may beneficially modulate pertinent cellular and molecular pathways. We aimed to provide an integrative overview of mechanisms of DMD pathology that may improve or worsen as a result of exercise. We also sought to stimulate discussion of what outcomes/dependent variables most appropriately measure these mechanisms, with the purpose of defining criteria for well-designed, controlled studies of exercise in DMD. The five mechanisms include pathways that are both intrinsic and extrinsic to the diseased muscle cells.

show abstract

Section: Increased Oxidative Stresssupporting

confidence: 78%

Exercise and duchenne muscular dystrophy: Toward evidence‐based exercise prescription

et al. 2011

View full text Add to dashboard Cite

show abstract

“…Recent results on patients with Duchenne muscular dystrophy indicate a significant increase of lipid peroxidation in muscle samples (8, 14) but not in erythrocytes (14). In the present study alterations in the activities of enzymatic antioxidants, glutathione peroxidase and catalase, proved to be of a minor nature.…”

Section: Discussionsupporting

confidence: 49%

Activities of some antioxidative and hexose monophosphate shunt enzymes of skeletal muscle in neuromuscular diseases

Myllylä

Kihlström

Takala

et al. 1986

Acta Neurologica Scandinavica

View full text Add to dashboard Cite

The activities of some antioxidative and hexose monophosphate shunt enzymes, as well as of 2 hydrolases were studied in skeletal muscle biopsy specimens taken from 39 patients with neuromuscular diseases and from 15 controls. The activity of Se-dependent glutathione peroxidase was higher in patients with congenital myotonia, whereas in the other diagnostic groups this enzyme activity was the same as in the controls. The Se-independent and total glutathione peroxidase activity of patients in the various diagnostic groups did not differ from the controls. Moreover, no difference were observed in catalase activity between the patient groups and the controls. The activities of the rate limiting enzymes of hexose monophosphate shunt, glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase of muscle biopsy samples of various patient groups did not show any significant difference from controls. The activity of a lysosomal hydrolase, beta-N-acetylglucosaminidase, was increased in patients with polyneuropathy and the activity of a nonlysosomal protease, alkaline protease, was high in patients with Charcot-Marie-Tooth disease. The activities of Se-dependent glutathione peroxidase, 6-phosphogluconate dehydrogenase and of both hydrolases showed a significant correlation to the magnitude of muscle atrophy.

show abstract

“…Elevated levels of secondary ROS and RNS can damage membrane lipids, structural and regulatory proteins, and DNA. Increased levels of lipid and protein oxidation have been reported in dystrophic muscle of patients with DMD (Haycock et al, 1996; Kar and Pearson, 1979; Mechler et al, 1984) and animal models of muscular dystrophy (Disatnik et al, 1998; Hauser et al, 1995; Mizuno, 1984; Terrill et al, 2013) indicating that oxidative stress could be an important regulator of muscle wasting in DMD.…”

Section: Oxidative Stressmentioning

confidence: 99%

Wasting mechanisms in muscular dystrophy

Shin

Tajrishi

Ogura

et al. 2013

The International Journal of Biochemistry & Cell Biology

126

138

View full text Add to dashboard Cite

Muscular dystrophy is a group of more than 30 different clinical genetic disorders that are characterized by progressive skeletal muscle wasting and degeneration. Primary deficiency of specific extracellular matrix, sarcoplasmic, cytoskeletal, or nuclear membrane protein results in several secondary changes such as sarcolemmal instability, calcium influx, fiber necrosis, oxidative stress, inflammatory response, breakdown of extracellular matrix, and eventually fibrosis which leads to loss of ambulance and cardiac and respiratory failure. A number of molecular processes have now been identified which hasten disease progression in human patients and animal models of muscular dystrophy. Accumulating evidence further suggests that aberrant activation of several signaling pathways aggravate pathological cascades in dystrophic muscle. Although replacement of defective gene with wild-type is paramount to cure, management of secondary pathological changes has enormous potential to improving the quality of life and extending lifespan of muscular dystrophy patients. In this article, we have reviewed major cellular and molecular mechanisms leading to muscle wasting in muscular dystrophy.

show abstract

Lipid peroxidation and superoxide dismutase activity in muscle and erythrocytes in Duchenne muscular dystrophy

Cited by 55 publications

References 13 publications

Exercise and duchenne muscular dystrophy: Toward evidence‐based exercise prescription

Exercise and duchenne muscular dystrophy: Toward evidence‐based exercise prescription

Activities of some antioxidative and hexose monophosphate shunt enzymes of skeletal muscle in neuromuscular diseases

Wasting mechanisms in muscular dystrophy

Contact Info

Product

Resources

About