A comparative investigation into the effect of chronic alcohol feeding on the myocardium of normotensive and hypertensive rats: An electrophoretic and biochemical study

Patel, Vinood B.; Sandhu, Gurjinder; Corbett, Joseph M.; Dünn, Michael J.; Rodrigues, L. M.; Griffiths, John R.; Wassif, Wassif; Sherwood, Roy; Richardson, Peter J.; Preedy, Victor R.

doi:10.1002/1522-2683(20000701)21:12<2454::aid-elps2454>3.0.co;2-z

Cited by 16 publications

(9 citation statements)

References 45 publications

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“…We have provided evidence that long‐term exposure of rats to a diet containing ethanol results in lower cellular content of both actin and α‐myosin heavy chain isoform and an increase in the β‐myosin heavy chain isoform (Vary and Deiter, 2005) (Table 1). Similarly, both Patel and colleagues (2000) and Figueredo and colleagues (1998) showed decreases in actin and α‐myosin heavy chain isoform, whereas Piano et al. showed chronic ethanol consumption induces an increase in the β‐myosin heavy chain isoform (Meehan et al., 1999).…”

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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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

View full text Add to dashboard Cite

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“…In the hearts of dogs and rats chronically fed with ethanol, myocardial ATP content was reported to be decreased 24 26 or unchanged 27,28 at estimated ethanol concentrations of 10 to 30 mM 29,30 . Similar findings have been obtained in studies with mitochondria from the liver 31,32 and brain 33 , where the maximum blood ethanol concentration is presumed to be no more than 30 mM.…”

Section: Discussionmentioning

confidence: 99%

Ethanol Dose- and Time-dependently Increases α and β Subunits of Mitochondrial ATP Synthase of Cultured Neonatal Rat Cardiomyocytes

2015

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Mitochondria are target subcellular organelles of ethanol. In this study, the effects of ethanol on protein composition was examined with 2-dimensional electrophoresis of protein extracts from cultured neonatal rat cardiomyocytes exposed to 100 mM ethanol for 24 hours. A putative β subunit of mitochondrial ATP synthase was increased, which was confirmed by Western blot. The cellular protein abundances in the α and β subunits of ATP synthase increased in dose (0, 10, 50, and 100 mM)-and time (0.5 hour and 24 hours)-dependent manners. The DNA microarray analysis of total RNA extract demonstrated that gene expression of the corresponding messenger RNAs of these subunit proteins did not significantly alter due to 24-hour ethanol exposure. Therefore, protein expression of these nuclear-encoded mitochondrial proteins may be regulated at the translational, rather than the transcriptional, level. Alternatively, degradation of these subunit proteins might be decreased. Additionally, cellular ATP content of cardiomyocytes scarcely decreased following 24-hour exposure to any examined concentrations of ethanol.Previous studies, together with this study, have demonstrated that protein abundance of the α subunit or β subunit or both subunits of ATP synthase after ethanol exposure or dysfunctional conditions might differ according to tissue: significant increases in heart but decreases in liver and brain. Thus, it is suggested that the abundance of subunit proteins of mitochondrial ATP synthase in the ethanol-exposed heart, being different from that in the liver and brain, should increase dose-dependently through either translational upregulation or decreased degradation or both to maintain ATP production, as the heart requires much more energy than other tissues for continuing sustained contractions. (J Nippon Med Sch 2015; 82: 237 245)

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“…Ultrastructural disarray of the contractile apparatus [74] is associated with a depressed myofibrillar and sarcoplasmic protein synthesis in cardiac muscle after ethanol exposure [75–77]. This reduces contractile cardiac filaments with subsequent negative inotropic effects on heart contractility [78, 79]. An apoptotic effect of ethanol on cardiac muscle has also been described, which could be counteracted by insulin-like growth factor (IGF)-I [80] and confirmed in later studies [81, 82].…”

Section: Alcoholic Cardiomyopathy: Cytotoxicity Of Alcohol On Heart Mmentioning

confidence: 99%

Alcoholic cardiomyopathy

Maisch

2016

Herz

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The individual amount of alcohol consumed acutely or chronically decides on harm or benefit to a person’s health. Available data suggest that one to two drinks in men and one drink in women will benefit the cardiovascular system over time, one drink being 17.6 ml 100 % alcohol. Moderate drinking can reduce the incidence and mortality of coronary artery disease, heart failure, diabetes, ischemic and hemorrhagic stroke. More than this amount can lead to alcoholic cardiomyopathy, which is defined as alcohol toxicity to the heart muscle itself by ethanol and its metabolites. Historical examples of interest are the Munich beer heart and the Tübingen wine heart. Associated with chronic alcohol abuse but having different etiologies are beriberi heart disease (vitamin B1 deficiency) and cardiac cirrhosis as hyperdynamic cardiomyopathies, arsenic poising in the Manchester beer epidemic, and cobalt intoxication in Quebec beer drinker’s disease. Chronic heavy alcohol abuse will also increase blood pressure and cause a downregulation of the immune system that could lead to increased susceptibility to infections, which in turn could add to the development of heart failure. Myocardial tissue analysis resembles idiopathic cardiomyopathy or chronic myocarditis. In the diagnostic work-up of alcoholic cardiomyopathy, the confirmation of alcohol abuse by carbohydrate deficient transferrin (CDT) and increased liver enzymes, and the involvement of the heart by markers of heart failure (e.g., NT-proBNP) and of necrosis (e.g., troponins or CKMb) is mandatory. Treatment of alcoholic cardiomyopathy consists of alcohol abstinence and heart failure medication.

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A comparative investigation into the effect of chronic alcohol feeding on the myocardium of normotensive and hypertensive rats: An electrophoretic and biochemical study

Cited by 16 publications

References 45 publications

Impact of Chronic Alcohol Ingestion on Cardiac Muscle Protein Expression

Impact of Chronic Alcohol Ingestion on Cardiac Muscle Protein Expression

Ethanol Dose- and Time-dependently Increases α and β Subunits of Mitochondrial ATP Synthase of Cultured Neonatal Rat Cardiomyocytes

Alcoholic cardiomyopathy

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