Ethanol Induced Morphologic Alterations During Growth and Maturation of Cardiac Myocytes

Adickes, Edward D.; Mollner, Teresa J.; Lockwood, Susan K.

doi:10.1111/j.1530-0277.1990.tb01822.x

Cited by 23 publications

(9 citation statements)

References 24 publications

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“…Thus, acute and short term exposures appear to decrease cell proliferation by 40-50% in all models reported to date (Jang et al, 2002a,b,c;Nixon and Crews, 2002;Rice et al, 2004). These data are consistent with reports that alcohol inhibits cell proliferation in many cell types, including but not limited to liver, bone, ovary, and other stem cells (Adickes et al, 1990;Cook et al, 1990;Cook and Keiner, 1991;Friday and Howard, 1991;Ahluwalia et al, 1995;Zimmerman et al, 1995).…”

Section: Alcohol Inhibition Of Adult Neurogenesis: Different Mechanissupporting

confidence: 84%

Alcohol and adult neurogenesis: Roles in neurodegeneration and recovery in chronic alcoholism

2006

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The concept of "structural plasticity" has emerged as a potential mechanism in neurodegenerative and psychiatric diseases such as drug abuse, depression, and dementia. Chronic alcoholism is a progressive neurodegenerative disease while the person continues to abuse alcohol, though clinical and imaging studies show that some recovery may occur with abstinence. The neural plasticity observed in chronic alcoholism coupled with conflicting reports on alcohol-induced hippocampal neuropathology make this disease ripe for reconsideration in terms of the phenomenon of adult neurogenesis. This review describes opposing neurogenic processes that occur with alcohol intoxication and abstinence following alcohol dependence and how these opposing events relate to neurodegeneration and recovery from chronic alcoholism.

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Section: Alcohol Inhibition Of Adult Neurogenesis: Different Mechanissupporting

confidence: 84%

Alcohol and adult neurogenesis: Roles in neurodegeneration and recovery in chronic alcoholism

2006

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“…37 This was originally proposed by Schreiber and colleagues 38 -39 who found that the synthesis of myocardial proteins in vitro was unaffected by physiological levels of ethanol (50 mmol/1) although supra-physiological concentrations 040 mmol/1) were inhibitory. Certainly in vitro studies on myocytes have shown that ethanol reduces the number and uniformity of the myofibrils.…”

Section: Synthesis Of Contractile Proteinsmentioning

confidence: 93%

Ethanol induced cardiovascular disease

Preedy

Richardson

1994

British Medical Bulletin

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Although the beneficial effects of mild or moderate ethanol consumption have been implied with respect to coronary artery disease, excessive ethanol consumption can result in alcoholic heart muscle disease (AHMD). The latter is characterized by features consistent with dilated cardiomyopathy with concomitant ventricular dysfunction and histopathological abnormalities. By definition, no other cause for the abnormalities in AHMD is demonstrated, other than excessive alcohol consumption. The metabolic basis of AHMD is probably multi-factorial, and the alterations of myocardial biochemistry are contributing factors for the precipitation and progression of the disease. The latter may reverse with abstention. Evidence is provided to support the contention that the abnormalities include central defects in protein metabolism, which perhaps are engendered by free radicals and/or the formation of acetaldehyde adducts. The latter may initiate the formation of auto-antibodies, therefore providing an auto-immune basis for AHMD in chronic alcohol misuse. Evidence is also provided to show that acetaldehyde is a potent perturbant of protein synthesis, and reduces the formation of new contractile proteins.

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“…Microscopic examination of biopsy specimens obtained from humans reveals myocyte degeneration, loss of striations, and myofilament dissolution, consistent with alterations in structural and myofibrillar proteins (Alexander, 1966a,b; Bulloch et al., 1972; Ferrans et al., 1975; Hibbs et al., 1965). Addition of ethanol to the medium reduces the number and uniformity of the myofibrils of myocytes in culture (Adickes et al., 1990). The process of alterations in ethanol‐induced cardiac structure and function is referred to as alcoholic heart muscle disease.…”

Section: Changes In Myocardial Proteins With Chronic Alcohol Intoxicmentioning

confidence: 99%

Impact of Chronic Alcohol Ingestion on Cardiac Muscle Protein Expression

Fogle¹,

Lynch²,

Palopoli³

et al. 2010

Alcoholism Clin & Exp Res

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Background Chronic alcohol abuse contributes not only to an increased risk of health-related complications, but also to a premature mortality in adults. Myocardial dysfunction, including the development of a syndrome referred to as alcoholic cardiomyopathy, appears to be a major contributing factor. One mechanism to account for the pathogenesis of alcoholic cardiomyopathy involves alterations in protein expression secondary to an inhibition of protein synthesis. However, the full extent to which myocardial proteins are affected by chronic alcohol consumption remains unresolved. Methods The purpose of this study was to examine the effect of chronic alcohol consumption on the expression of cardiac proteins. Male rats were maintained for 16 weeks on a 40% ethanol-containing diet in which alcohol was provided both in drinking water and agar blocks. Control animals were pair-fed to consume the same caloric intake. Heart homogenates from control- and ethanol-fed rats were labeled with the cleavable isotope coded affinity tags (ICAT™). Following the reaction with the ICAT™ reagent, we applied one-dimensional gel electrophoresis with in-gel trypsin digestion of proteins and subsequent MALDI-TOF-TOF mass spectrometric techniques for identification of peptides. Differences in the expression of cardiac proteins from control- and ethanol-fed rats were determined by mass spectrometry approaches. Results Initial proteomic analysis identified and quantified hundreds of cardiac proteins. Major decreases in the expression of specific myocardial proteins were observed. Proteins were grouped depending on their contribution to multiple activities of cardiac function and metabolism, including mitochondrial-, glycolytic-, myofibrillar-, membrane-associated, and plasma proteins. Another group contained identified proteins that could not be properly categorized under the aforementioned classification system. Conclusions Based on the changes in proteins, we speculate modulation of cardiac muscle protein expression represents a fundamental alteration induced by chronic alcohol consumption, consistent with changes in myocardial wall thickness measured under the same conditions.

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Ethanol Induced Morphologic Alterations During Growth and Maturation of Cardiac Myocytes

Cited by 23 publications

References 24 publications

Alcohol and adult neurogenesis: Roles in neurodegeneration and recovery in chronic alcoholism

Alcohol and adult neurogenesis: Roles in neurodegeneration and recovery in chronic alcoholism

Ethanol induced cardiovascular disease

Impact of Chronic Alcohol Ingestion on Cardiac Muscle Protein Expression

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