Effect of Chronic Ethanol Ingestion on Liver and Plasma Protein Synthesis in Galactosamine-induced Hepatitis in Rats

1. An investigation was carried out into the response of soluble, myofibrillar and stromal protein fractions of skeletal muscle to chronic ethanol feeding. Groups of male Wistar rats, of approx. 85 or 280 g body wt., were pair-fed on a nutritionally complete liquid diet containing glucose or a diet in which 36% of the total energy was provided by ethanol. After 6 weeks, rates of protein synthesis were measured with a flooding dose of L-[4-3H]phenylalanine. 2. The protein contents of soluble, myofibrillar and stromal fractions in gastrocnemius muscle from small and large rats were decreased by ethanol feeding. Greater changes were observed in small than in large rats. 3. Fractional synthesis rates of soluble, myofibrillar and stromal proteins of gastrocnemius were all decreased by ethanol treatment. All fractions responded similarly, though percentage decreases in large rats were greater than in small rats. Absolute synthesis rates in gastrocnemius muscles were also decreased after ethanol treatment. All protein fractions responded similarly, and the magnitudes of the responses in large and small rats were also similar. 4. Fractional rates of breakdown, measured by the difference between fractional growth and synthesis rates, were apparently decreased, in both sets of rats, in all protein fractions. 5. It was concluded that chronic ethanol exposure causes perturbations in soluble, myofibrillar and stromal protein accretion by a mechanism involving unidirectional changes in protein synthesis and possibly breakdown.

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Effect of Chronic Ethanol Ingestion on Mitochondrial Protein Synthesis in Sinclair(S-l) Miniature Swine

Experimental Biology and Medicine ◽

10.3181/00379727-148-38687 ◽

1975 ◽

Vol 148 (4) ◽

pp. 1051-1056 ◽

Cited By ~ 8

Author(s):

J. P. Burke ◽

M. E. Tumbleson ◽

K. W. Hicklin ◽

R. B. Wilson

Keyword(s):

Protein Synthesis ◽

Mitochondrial Protein ◽

Chronic Ethanol ◽

Ethanol Ingestion ◽

Mitochondrial Protein Synthesis ◽

Miniature Swine

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The effect of chronic ethanol ingestion on protein metabolism in type-I- and type-II-fibre-rich skeletal muscles of the rat

Biochemical Journal ◽

10.1042/bj2540631 ◽

1988 ◽

Vol 254 (3) ◽

pp. 631-639 ◽

Cited By ~ 69

Author(s):

V R Preedy ◽

T J Peters

Keyword(s):

Protein Synthesis ◽

Protein Metabolism ◽

Skeletal Muscle Fibre ◽

Chronic Ethanol ◽

Ethanol Ingestion ◽

Type I ◽

Type Ii ◽

Ethanol Feeding ◽

Dna 2 ◽

Rna And Dna

1. The effects of chronic ethanol feeding on muscles containing a predominance of either Type I (aerobic, slow-twitch) or Type II (anaerobic, fast-twitch) fibres were studied. Male Wistar rats, weighing approx. 90 g or 280 g, were pair-fed on a nutritionally complete liquid diet containing 36% of total energy as ethanol, or isovolumetric amounts of the same diet in which ethanol was replaced by isoenergetic glucose. After 6 weeks feeding, fractional rates of protein synthesis were measured with a flooding dose of L-[4-(3)H]-phenylalanine and muscles were analysed for protein, RNA and DNA. 2. Ethanol feeding decreased muscle weight, protein, RNA and DNA contents in both small and large rats. Type-II-fibre-rich muscles showed greater changes than did Type-I-fibre-rich muscles. Changes in protein paralleled decreases in DNA. 3. The capacity for protein synthesis (RNA/protein), fractional rates of protein synthesis and absolute rates of protein synthesis were decreased by ethanol feeding in both small and large rats. The amounts of protein synthesized relative to RNA and DNA were also decreased. Changes were less marked in Type-I than in Type-II-fibre-rich muscles. Loss of protein, RNA and DNA was greater in small rats, but protein synthesis was more markedly affected in large rats. 4. It was concluded that chronic ethanol feeding adversely affects protein metabolism in skeletal muscle. Fibre composition and animal size are also important factors in determining the pattern of response.

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Factors Regulating Plasma Protein Synthesis IV. Influence of Fragments D and E on Plasma Fibrinogen Concentration

Thrombosis and Haemostasis ◽

10.1055/s-0038-1649178 ◽

1974 ◽

Vol 31 (03) ◽

pp. 395-402 ◽

Cited By ~ 7

Author(s):

V Bocci ◽

T Conti ◽

M Muscettola ◽

A Pacini ◽

G. P Pessina

Keyword(s):

Protein Synthesis ◽

Plasma Protein ◽

Plasma Fibrinogen ◽

Fibrinogen Concentration

SummaryRabbit fibrinogen digest products (FDP) have been separated by Pevikon block electrophoresis yielding fragments D, E and other unidentified FDP.The fragments were injected into rabbits. Surprisingly, as little as 4.3 mg of fragment D elicited a significant increase in plasma fibrinogen concentration 24 hr after injection. The stimulating activity of fragment D is at least 10-fold higher than that of fragment E.

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Chronic Alcoholism Decreases Polyunsaturated Fatty Acid Levels in Human Plasma, Erythrocytes, and Platelets – Influence of Chronic Liver Disease

Thrombosis and Haemostasis ◽

10.1055/s-0038-1657633 ◽

1997 ◽

Vol 78 (02) ◽

pp. 808-812 ◽

Cited By ~ 10

Author(s):

María-Luisa Pita ◽

José-María Rubio ◽

María-Luisa Murillo ◽

Olimpia Carreras ◽

Mariá-José Delgado

Keyword(s):

Fatty Acid ◽

Liver Disease ◽

Chronic Liver Disease ◽

Chronic Alcoholism ◽

Chronic Liver ◽

Chronic Ethanol ◽

Ethanol Ingestion ◽

Control Group ◽

Docosatetraenoic Acid ◽

Long Chain

SummaryThe effect of chronic ethanol ingestion on fatty acid composition of plasma, erythrocyte and platelet phospholipids and on plasma 6-keto-PGF1α was studied. Two groups of alcoholic subjects, one of them with chronic liver disease, were studied and compared to a control group of healthy subjects. Linoleic acid was not affected by alcoholism but its larger metabolites arachidonic acid (20:4n6) and docosatetraenoic acid (22: 4n6) tended to be lower in erythrocytes and platelets of both groups of alcoholic patients; the decrease was more marked in the presence of chronic liver disease. Docosahexaenoic acid (22:6n3) was markedly decreased in plasma, erythrocytes and platelets obtained from alcoholic patients with chronic liver disease. Plasma levels of 6-keto-PGF1α, a metabolite of prostacyclin (PGI2), remained unchanged. We conclude that chronic ethanol ingestion induces important changes in long-chain polyunsaturated fatty acids, mainly in platelets, and that these changes are exacerbated when patients suffer from chronic liver disease.

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