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Biomedical subjects

M Anton

Publications and source records attributed to M Anton.

At least 91 records · Page 5Linked to original sources
PubMed1982

Protective effect of colectomy in frog virus 3 hepatitis of rats: possible role of endotoxin.

Four to six days after colectomy, rats resisted a challenge of frog virus 3 that in sham-operated animals led to lethal hepatitis. Furthermore, the beneficial effect of colectomy was lost after intravenous administration of a dose of bacterial endotoxin as small as 0.01 100% lethal dose. The protection was related to neither a different distribution of the virus in body organs nor a stimulation of the reticuloendothelial system. The virus-induced early events--destruction of liver sinusoidal cells with leakage of cathepsin D into serum and inhibition of liver macromolecular synthesis--evolved similarly in both groups of rats. After an identical consumption of complement at the beginning of infection, a renewal in complement activity in the protected rats contrasted with an increasing deficiency in the control animals. The protective role of colectomy seems to be related to the suppression of the main source of bacterial endotoxin.

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PubMed1981

Frog virus 3 induces a fatal hepatitis in rats.

To define its pathogenesis, the acute degenerative hepatitis caused by frog virus 3 (FV3) has been reproduced in the rat, thus facilitating a greater number of biologic explorations than in the mouse. The histologic and ultrastructural study proves a massive hepatocellular necrosis perfectly compatible with the fatal outcome of the illness 30 hours after the inoculation of one LD100. Critical analysis of the FV3 rat hepatitis induces us to advance three arguments for excluding the direct role of the virus in hepatocytolysis. (1) The hepatocyte is neither the sole nor the first intrahepatic target of the virus. The endothelial barrier and especially the Kupffer cells are completely necrosed several hours prior to the appearance of the first signs of parenchymal cell disturbances. Morphologic observations and, in particular, the evolution in the site and chronology of the cytolysis are confirmed by the variation in the activity of cathepsin D, glutamic pyruvic transaminase, and lactic dehydrogenase in serum. (2) There is a close correlation between the structural alterations in the hepatocyte nuclei and the inhibition in the synthesis of the liver macromolecules. But the discovery of a rat strain sensitive to the virus and another more resistant strain provides evidence that there is no relationship between the sensitivity to the lethal power of the FV3 and the metabolic disorders. (3) The ways in which the FV3 spreads throughout the organism do not explain why the liver is the sole organ attacked. A second etiopathogenic factor, only found in the liver, must be invoked. The possible role of the plasma complement, strongly activated, is suggested, along with that of other toxic substances which can no longer be cleared. The metabolic inhibition directly connected with the FV3 would thus result not in producing the hepatocytolysis but in rendering any cellular regeneration impossible.

Animals↗
PubMed1979

[Protection of mice with bacterial phospholipids against the lethal effect of Frog Virus 3 (FV 3) (author's transl)].

A bacterial phospholipid extract (EBP) inoculated intraveinously at a dose of 1 mg/25 g body weight 30 hours before infection protects mice against the lethal effect of Frog Virus 3 (FV 3). The anti-FV 3 resistance produced by EBP requires protein synthesis during the period of pretreatment. The treatment with the bacterial extract has no effect on the inhibition of the macromolecular synthesis of the liver (RNA and DNA) which is observed at the beginning of the infection. However 48 hours after FV 3 infection, there is a notable stimulation of DNA synthesis which probably corresponds to liver regeneration.

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PubMed1978

Phagocytic properties displayed by mouse hepatocytes after virus induced damage of the sinusoidal lining.

Frog virus 3 (FV 3) inoculated intravenously into mice damages sinusoidal cells and produces a decrease in the carbon uptake capacity of the liver. Histological and ultrastructural examinations have shown that in FV 3 infected animals part of the inoculated carbon is taken up by the hepatocytes and can be located inside cytoplasmic vesicles or dense bodies. The hepatocytes are also able to phagocyte latex particles of 312 nm in diameter. These observations demonstrate that once the Kupffer cells and the endothelial lining are damaged, hepatocytes can display phagocytic properties.

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