Oxidative stress and pathology in muscular dystrophies: focus on protein thiol oxidation and dysferlinopathies

The muscular dystrophies comprise more than 30 clinical disorders that are characterized by progressive skeletal muscle wasting and degeneration. Although the genetic basis for many of these disorders has been identified, the exact mechanism for pathogenesis generally remains unknown. It is consider...

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Main Authors: Terrill, J., Radley-Crabb, Hannah, Iwasaki, T., Lemckert, F., Arthur, P., Grounds, M.
Format: Journal Article
Published: Blackwell Publishing 2013
Subjects:
Online Access:http://hdl.handle.net/20.500.11937/33827
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author Terrill, J.
Radley-Crabb, Hannah
Iwasaki, T.
Lemckert, F.
Arthur, P.
Grounds, M.
author_facet Terrill, J.
Radley-Crabb, Hannah
Iwasaki, T.
Lemckert, F.
Arthur, P.
Grounds, M.
author_sort Terrill, J.
building Curtin Institutional Repository
collection Online Access
description The muscular dystrophies comprise more than 30 clinical disorders that are characterized by progressive skeletal muscle wasting and degeneration. Although the genetic basis for many of these disorders has been identified, the exact mechanism for pathogenesis generally remains unknown. It is considered that disturbed levels of reactive oxygen species (ROS) contribute to the pathology of many muscular dystrophies. Reactive oxygen species and oxidative stress may cause cellular damage by directly and irreversibly damaging macromolecules such as proteins, membrane lipids and DNA; another major cellular consequence of reactive oxygen species is the reversible modification of protein thiol side chains that may affect many aspects of molecular function. Irreversible oxidative damage of protein and lipids has been widely studied in Duchenne muscular dystrophy, and we have recently identified increased protein thiol oxidation in dystrophic muscles of the mdx mouse model for Duchenne muscular dystrophy. This review evaluates the role of elevated oxidative stress in Duchenne muscular dystrophy and other forms of muscular dystrophies, and presents new data that show significantly increased protein thiol oxidation and high levels of lipofuscin (a measure of cumulative oxidative damage) in dysferlin-deficient muscles of A/J mice at various ages. The significance of this elevated oxidative stress and high levels of reversible thiol oxidation, but minimal myofibre necrosis, is discussed in the context of the disease mechanism for dysferlinopathies, and compared with the situation for dystrophin-deficient mdx mice.
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spelling curtin-20.500.11937-338272017-09-13T15:32:49Z Oxidative stress and pathology in muscular dystrophies: focus on protein thiol oxidation and dysferlinopathies Terrill, J. Radley-Crabb, Hannah Iwasaki, T. Lemckert, F. Arthur, P. Grounds, M. N-acetylcysteine Dysferlinopathies antioxidants reactive oxygen species Duchenne muscular dystrophy dystropathology muscle necrosis skeletal muscle protein thiol oxidation oxidative stress The muscular dystrophies comprise more than 30 clinical disorders that are characterized by progressive skeletal muscle wasting and degeneration. Although the genetic basis for many of these disorders has been identified, the exact mechanism for pathogenesis generally remains unknown. It is considered that disturbed levels of reactive oxygen species (ROS) contribute to the pathology of many muscular dystrophies. Reactive oxygen species and oxidative stress may cause cellular damage by directly and irreversibly damaging macromolecules such as proteins, membrane lipids and DNA; another major cellular consequence of reactive oxygen species is the reversible modification of protein thiol side chains that may affect many aspects of molecular function. Irreversible oxidative damage of protein and lipids has been widely studied in Duchenne muscular dystrophy, and we have recently identified increased protein thiol oxidation in dystrophic muscles of the mdx mouse model for Duchenne muscular dystrophy. This review evaluates the role of elevated oxidative stress in Duchenne muscular dystrophy and other forms of muscular dystrophies, and presents new data that show significantly increased protein thiol oxidation and high levels of lipofuscin (a measure of cumulative oxidative damage) in dysferlin-deficient muscles of A/J mice at various ages. The significance of this elevated oxidative stress and high levels of reversible thiol oxidation, but minimal myofibre necrosis, is discussed in the context of the disease mechanism for dysferlinopathies, and compared with the situation for dystrophin-deficient mdx mice. 2013 Journal Article http://hdl.handle.net/20.500.11937/33827 10.1111/febs.12142 Blackwell Publishing unknown
spellingShingle N-acetylcysteine
Dysferlinopathies
antioxidants
reactive oxygen species
Duchenne muscular dystrophy
dystropathology
muscle necrosis
skeletal muscle
protein thiol oxidation
oxidative stress
Terrill, J.
Radley-Crabb, Hannah
Iwasaki, T.
Lemckert, F.
Arthur, P.
Grounds, M.
Oxidative stress and pathology in muscular dystrophies: focus on protein thiol oxidation and dysferlinopathies
title Oxidative stress and pathology in muscular dystrophies: focus on protein thiol oxidation and dysferlinopathies
title_full Oxidative stress and pathology in muscular dystrophies: focus on protein thiol oxidation and dysferlinopathies
title_fullStr Oxidative stress and pathology in muscular dystrophies: focus on protein thiol oxidation and dysferlinopathies
title_full_unstemmed Oxidative stress and pathology in muscular dystrophies: focus on protein thiol oxidation and dysferlinopathies
title_short Oxidative stress and pathology in muscular dystrophies: focus on protein thiol oxidation and dysferlinopathies
title_sort oxidative stress and pathology in muscular dystrophies: focus on protein thiol oxidation and dysferlinopathies
topic N-acetylcysteine
Dysferlinopathies
antioxidants
reactive oxygen species
Duchenne muscular dystrophy
dystropathology
muscle necrosis
skeletal muscle
protein thiol oxidation
oxidative stress
url http://hdl.handle.net/20.500.11937/33827