[<sup>3</sup>H]‐OUABAIN BINDING TO PERIPHERAL ORGANS OF CATS: EFFECT OF ETHANOL

Banerjee, Sipra; Sharma, Virendra K.

doi:10.1111/j.1476-5381.1978.tb07750.x

Cited by 6 publications

(1 citation statement)

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“…With respect to animal studies, there are good models for acute alcohol‐induced muscle damage, mainly in rodents (Preedy et al., 1990). Other animal models of ethanol‐induced muscle damage include the use of dogs and cats (Barnejee and Sharma, 1978; Ferguson et al., 1984). However, animal models are arguably of limited value in the chronic model of skeletal myopathy, because the precise changes are not the same as those in human alcoholic myopathy (Fernandez‐Solà et al., 1996).…”

Section: Historical Timeline Events In Alcoholic Myopathiesmentioning

confidence: 99%

Molecular and Cellular Events in Alcohol‐Induced Muscle Disease

Fernández‐Solà

Preedy

Lang

et al. 2007

Alcoholism Clin & Exp Res

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Alcohol consumption induces a dose-dependent noxious effect on skeletal muscle, leading to progressive functional and structural damage of myocytes, with concomitant reductions in lean body mass. Nearly half of high-dose chronic alcohol consumers develop alcoholic skeletal myopathy. The pathogenic mechanisms that lie between alcohol intake and loss of muscle tissue involve multiple pathways, making the elucidation of the disease somewhat difficult. This review discusses the recent advances in basic and clinical research on the molecular and cellular events involved in the development of alcohol-induced muscle disease. The main areas of recent research interest on this field are as follows: (i) molecular mechanisms in alcohol exposed muscle in the rat model; (ii) gene expression changes in alcohol exposed muscle; (iii) the role of trace elements and oxidative stress in alcoholic myopathy; and (iv) the role of apoptosis and preapoptotic pathways in alcoholic myopathy. These aforementioned areas are crucial in understanding the pathogenesis of this disease. For example, there is overwhelming evidence that both chronic alcohol ingestion and acute alcohol intoxication impair the rate of protein synthesis of myofibrillar proteins, in particular, under both postabsorptive and postprandial conditions. Perturbations in gene expression are contributory factors to the development of alcoholic myopathy, as ethanol-induced alterations are detected in over 400 genes and the protein profile (i.e., the proteome) of muscle is also affected. There is supportive evidence that oxidative damage is involved in the pathogenesis of alcoholic myopathy. Increased lipid peroxidation is related to muscle fibre atrophy, and reduced serum levels of some antioxidants may be related to loss of muscle mass and muscle strength. Finally, ethanol induces skeletal muscle apoptosis and increases both pro- and antiapoptotic regulatory mechanisms.

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