Alcoholic muscle disease and biomembrane perturbations (review)

Adachi, Junko; Asano, Masaharu; Ueno, Yoshio; Niemelä, Onni; Ohlendieck, Kay; Peters, Timothy J.; Preedy, Victor R.

doi:10.1016/s0955-2863(03)00114-1

Cited by 57 publications

(35 citation statements)

References 76 publications

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“…Alcoholic myopathy is the most prevalent skeletal muscle disorder in the Western Hemisphere, as it occurs in 40–60 % of alcohol abusers [1, 119]. Since alcoholic myopathy arises in the presence or absence of polyneuropathy [98], the two disease processes should be evaluated independently.…”

Section: Neuromuscular Diseases In Alcoholicsmentioning

confidence: 99%

Human alcohol-related neuropathology

2013

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Alcohol-related diseases of the nervous system are caused by excessive exposures to alcohol, with or without co-existing nutritional or vitamin deficiencies. Toxic and metabolic effects of alcohol (ethanol) vary with brain region, age/developmental stage, dose, and duration of exposures. In the mature brain, heavy chronic or binge alcohol exposures can cause severe debilitating diseases of the central and peripheral nervous systems, and skeletal muscle. Most commonly, long-standing heavy alcohol abuse leads to disproportionate loss of cerebral white matter and impairments in executive function. The cerebellum (especially the vermis), cortical-limbic circuits, skeletal muscle, and peripheral nerves are also important targets of chronic alcohol-related metabolic injury and degeneration. Although all cell types within the nervous system are vulnerable to the toxic, metabolic, and degenerative effects of alcohol, astrocytes, oligodendrocytes, and synaptic terminals are major targets, accounting for the white matter atrophy, neural inflammation and toxicity, and impairments in synaptogenesis. Besides chronic degenerative neuropathology, alcoholics are predisposed to develop severe potentially life-threatening acute or subacute symmetrical hemorrhagic injury in the diencephalon and brainstem due to thiamine deficiency, which exerts toxic/metabolic effects on glia, myelin, and the microvasculature. Alcohol also has devastating neurotoxic and teratogenic effects on the developing brain in association with fetal alcohol spectrum disorder/fetal alcohol syndrome. Alcohol impairs function of neurons and glia, disrupting a broad array of functions including neuronal survival, cell migration, and glial cell (astrocytes and oligodendrocytes) differentiation. Further progress is needed to better understand the pathophysiology of this exposure-related constellation of nervous system diseases and better correlate the underlying pathology with in vivo imaging and biochemical lesions.

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Section: Neuromuscular Diseases In Alcoholicsmentioning

confidence: 99%

Human alcohol-related neuropathology

2013

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“…During the development process of alcohol-induced liver disease, PM plays an important role. Alcohol can increase the membrane permeability and induce membrane defects [6][7][8].…”

Section: Introductionmentioning

confidence: 99%

Plasma membrane proteome analysis of the early effect of alcohol on liver: implications for alcoholic liver disease

Zhang¹,

Jia²,

Feng³

et al. 2011

ABBS

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In humans, the over-consumption of alcohol can lead to serious liver disease. To examine the early effects of alcohol on liver disease, rats were given sufficient ethanol to develop liver cirrhosis. Rats before the onset of fibrosis were studied in this work. Plasma membranes (PM) of liver were extracted by twice sucrose density gradient centrifugation. The proteome profiles of PM from ethanol-treated rats and the controls were analyzed using two-dimensional gel electrophoresis (2-DE) and isobaric tag for relative and absolute quantitation (iTRAQ) technology. Ethanol treatment altered the amount of 15 different liver proteins: 10 of them were detected by 2-DE and 5 by iTRAQ. Keratin 8 was detected by both methods. Gene ontology analysis of these differentially detected proteins indicated that most of them were involved in important cell functions such as binding activity (including ion, DNA, ATP binding, etc.), cell structure, or enzyme activity. Among these, annexin A2, keratin 8, and keratin 18 were further verified using western blot analysis and annexin A2 was verified by immunohistochemistry. Our results suggested that alcohol has the potential to affect cell structure, adhesion and enzyme activity by altering expression levels of several relevant proteins in the PM. To the best of our knowledge, this is the first time to study the effect of alcohol on the liver PM proteome and it might be helpful for understanding the possible mechanisms of alcohol-induced liver disease.

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“…On the other hand, 25-hydroxy-and 26-hydroxy-cholesterol are [37]. Changes in skeletal muscle levels of 7-h-hydroxy-and 7-keto-cholesterol have been noted in alcoholic muscle disease, where muscle protein carbonyl levels were unchanged or even slightly diminished [38]. Serum ferritin level (an index of Fe status) has been shown to be positively correlated with levels of several oxysterols in humans [39].…”

Section: Discussionmentioning

confidence: 99%