Toxic liver injury. Inhibition of protein synthesis in rat liver by dimethylnitrosamine <i>in vivo</i>

Magee, Peter

doi:10.1042/bj0700606

Cited by 92 publications

(25 citation statements)

References 26 publications

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“…Studies of Magef. [6,7] and of ourselves have shown dimethylnitrosamine (DMNA) to specifically act upon the hepatic cells only.…”

mentioning

confidence: 99%

Comparative Study of Two Models for Experimental Cirrhosis in the Dog

Testas¹,

Benichou²,

Perrin³

et al. 1978

Eur Surg Res

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Two canine models of cirrhosis induced by administration of dimethylnitrosamine (DMNA) alone or in combination with hepatic vein ligation, were studied. The criteria used for development of cirrhosis were not only the appearance of portal hypertension, ascites, biochemical disorders or retention of BSP but also the formation of histological lesions such as sclerotic transformation of the liver lobules together with nodular regeneration. According to these criteria, the experimental protocol consisting in hepatic vein ligation and prolonged administration of DMNA was successful in inducing in animals liver cirrhosis similar to human conditions.

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“…Studies of Magef. [6,7] and of ourselves have shown dimethylnitrosamine (DMNA) to specifically act upon the hepatic cells only.…”

mentioning

confidence: 99%

Comparative Study of Two Models for Experimental Cirrhosis in the Dog

Testas¹,

Benichou²,

Perrin³

et al. 1978

Eur Surg Res

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“…As biochemical effects are only observed after a time-lag (Magee, 1958;Hultin et al 1960), and as decomposition in vivo is substantially confined to the liver, which is the only organ severely affected by acute doses (Magee, 1956), it has generally been assumed that the toxic compound is a metabolite. Formaldehyde (Brouwers & Emmelot 1960), nitrite (Heath & Dutton, 1958) and diazomethane (Rose, 1958;R.…”

mentioning

confidence: 99%

The decomposition and toxicity of dialkylnitrosamines in rats

Heath¹

1962

Biochemical Journal

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“…The increase in h protein level resulting from the feeding of diethylnitrosamine was paralleled by a considerable increase in the amount of isolable soluble liver proteins (Table III, column 3). This finding was unexpected since diethylnitrosamine and its methyl homolog, dimethylnitrosamine, are known to be potent inhibitors of protein synthesis both in vitro and in vivo as measured by the incorporation of radioactively labelled amino acids (Magee, 1958;Brouwers and Emmelot, 1960;Hultin, Arrhenius, Low and Magee, 1960). Two explanations may be offered.…”

Section: Administration Of Diethylnitrosaminementioning

confidence: 89%

A study of soluble protein and sulfhydryl levels in the rat liver during rapid normal and premalignant growth

Argus¹,

Walder²,

Fabian³

et al. 1968

Br J Cancer

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FOLLOWING the demonstration by Miller and Miller (1947) and Miller, Miller, Sapp and Weber (1949) that carcinogenic azo dyes are bound covalently to rat liver proteins before the appearance of tumors, the cytoplasmic h protein components of this combination (Sorof and Cohen, 1951; Wirtz and Arcos, 1958) have been extensively investigated. During liver carcinogenesis by the aminoazo dyes and by 2-acetylaminofluorene, the h2 liver proteins contain the greatest portion of the soluble carcinogen-protein conjugates (Sorof, Young and Ott, 1958;Sorof, Young and Fetterman, 1960), and there is at the time of maximum dye binding an increase in the total h protein fraction of the liver (Sorof, Young and Ott, 1958). In contrast, the primary tumors induced by these carcinogens do not form h2 protein-carcinogen conjugates (Sorof, Young McCue and Fetterman, 1963;Sorof, Young, McBride and Coffey, 1965), and the h fraction is considerably decreased in these hepatomas (Sorof and Cohen, 1951;Sorof, Young and Ott, 1958).It has been hypothesized that carcinogens combine with specific growthcontrolling proteins, the deletion of which gives rise to malignant cells (Miller and Miller, 1953; Potter, 1958), and certain h2 proteins of rat liver were postulated to be involved in regulation of cell multiplication (Bakay and Sorof, 1964). Freed and Sorof (1966) provided evidence that the h2 liver proteins do function in normal cells as metabolic regulators: isolated h2 protein fraction strongly inhibits the growth of L strain mouse fibroblasts in suspension tissue culture, and the inhibition of cell multiplication is reversed by removal of the h2 proteins. The inhibitory fraction centred at the slow h2 proteins has been recently identified as arginase (Sorof, Young, Luongo, Kish and Freed, 1967).The present investigations attempt to gain specific information on the possible role of the h proteins in the rapid normal growth of regenerating liver, in the rapid liver growth induced by polycyclic aromatic hydrocarbons, and in nitrosamine hepatocarcinogenesis. Thus, a study of the electrophoretic patterns of soluble rat liver proteins at various time intervals was carried out following partial hepatectomy and following intraperitoneal injection of a single dose of 20-methylcholanthrene. Electrophoretic patterns were also studied in soluble liver proteins obtained from rats which were continuously administered the hepatic carcinogen, diethylnitrosamine. The sulfhydryl levels in the soluble protein preparations and the mitotic indexes of the liver tissues were measured in order to correlate the electrophoretic patterns with these parameters of mitosis.

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Toxic liver injury. Inhibition of protein synthesis in rat liver by dimethylnitrosamine in vivo

Cited by 92 publications

References 26 publications

Comparative Study of Two Models for Experimental Cirrhosis in the Dog

Comparative Study of Two Models for Experimental Cirrhosis in the Dog

The decomposition and toxicity of dialkylnitrosamines in rats

A study of soluble protein and sulfhydryl levels in the rat liver during rapid normal and premalignant growth

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