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Mussel samples from four locations along the Norweigian coast were extracted by methods for diarrheic shellfish toxins (DST) and tested by chemical and biological methods, including histopathology. All samples had previously been found to be highly toxic in mice, with symptoms indicating the presence of non-diarrheagenic toxins in the mouse bioassay. Chemical analysis revealed that the DST okadaic acid (OA) and dinophysistoxin-1 (DTX1) were present each one in one sample, but only a minor part of the total toxicity could be attributed to these toxions. In the other two samples, OA and DTX1 were absent. Incubation of the mussel extracts from all four samples with freshly prepared hepatocytes indicated the presence of unknown toxin(s) which may not be classified within the DST complex. Purified mussel samples were given to baby mice both via intraperitoneal (i.p.) injections and by oral intubation. Oral toxicity was about 25-50 times lower than toxicity obtained by i.p. injections, a result in accordance with acute toxic properties of many toxins. Risk assessment of the unknown toxin(s) requires chemical identification, but the preliminary results obtained indicate a large margin of safety, based on the large amounts of mussel extracts necessary to yield toxic effects in the intestine and liver in experimental animals upon oral exposure versus human intake.

About 50 years ago crystalline deposits of a substance representing approximately 7 per cent wet tissue weight and believed to be hentriacontane or a mixture of similar long-chain n-alkanes (30-34 carbon atoms) were detected in two discoloured and swollen cow livers. Stored purified extracts from these livers were recently reanalysed using gas chromatography and mass spectrometry. They were found to contain about equal amounts of nonacosane and hentriacontane with a small admixture of tritriacontane and other long carbon-chain alkanes. On the basis of histological findings, five additional cases of "paraffin liver" in cows have been recorded. In the discussion comparison is made with the only known case of a similar disorder in a human, visceral accumulation of the same three alkanes as in the cows, which was recently described in the literature. Concerning the origin of the deposits, importance is given to the fact that the long-chain alkanes with odd carbon numbers identified both in cattle and man predominate in the cuticular waxes of many dietary plants. The very large quantities of the abnormal substance in the cow livers indicate low toxicity, and evidently accumulation over long periods of time.

Alveld is a hepatogenous photosensitization disease seen in lambs grazing Narthecium ossifragum pastures in Norway. Mycotoxins, possibly sporidesmin, have been suspected to cause the liver damage in alvled as in facial eczema. The histological changes in the liver of alveld cases and in lambs photosensitized after experimental sporidesmin intoxication were compared. The liver damage, characterized by necrosis in single centrilobular hepatocytes, was of the same type in both conditions. Minor to moderate portal fibroplasia and bile duct proliferation were almost always present. Accumulated glycogen was seen in hepatocytes in the centrilobular areas. This was significantly correlated to the enzymatically measured glycogen content and there was good correlation between parenchymal damage and glycogen accumulation. The glucose-6-phosphatase and glycogen phosphorylase activities were normal. These findings indicate that parenchymal damage, rather than obstruction of the bile ducts, caused the retention of phylloerythrin both in alveld cases and in experimentally sporidesmin-intoxicated lambs. The accumulation of glycogen could not be explained.

Sheep livers with environmental pigmentation were examined histochemically and by electron microscopy. The pigment granules in hepatocytes and Kupffer cells had abundant lipid droplets; they were interpreted as being a variant of lipofuscins. It is concluded that the presently used descriptive term for the condition, "perilobular liver melanosis" should be replaced by the expression "liver lipofuscinosis".

The patho-morphological lesions in the liver in late stages of canine endotoxin shock were studied by light and electron microscopy. Light microscopic lesions included sinusoidal dilatations, with accumulation of red cells and leucocytes, varying damage of the sinusoidal lining, microthrombi and widening of the space of Disse. Necrotic foci were in some cases recognized within a varying number of lobuli, at times in the centrilobular areas. Electron microscopy revealed severe hepatocytic damage. These lesions included formation of blebs and other surface protrusions corresponding to cytoplasmic ecdysis. The resulting cytoplasmic fragments seemed frequently to enter the sinusoids. It is suggested that the severe disturbances observed in the proteolytic enzyme systems of plasma during endotoxin shock are influenced by the hepatic parenchymal changes observed.

Two AA proteins were isolated from the same amyloid fibril preparation from the liver of a mink, in which amyloidosis had been induced by injections with endotoxin. The two proteins were of different size, one containing 53 amino acid residues and the other 64 residues. The amino acid sequence was otherwise found to be identical. Both proteins revealed pyrrolidone carboxylic acid as the N-terminal amino acid. Sequence homologies with protein AA from other species were very striking. However, no antigenic cross-reaction was seen between mink protein AA and antisera to protein AA from human, mouse or rabbit sources.

Liver phagocytosis was studied by means of electron microscopy in late stages of lethal canine endotoxin shock. A massive phagocytic activity was found within hepatic macrophages. The phagocytosed material found within Kupffer cells consisted of red cells, red-cell fragments, platelets, a fibrin-like material and damaged polymorphonuclear leukocytes. Red cells and red-cell fragments seemed to constitute the major part of the material involved.

In the familial form of hyperlipoproteinaemia type I of mink ( Mustela vison), mesenteric lipogranulomas are common findings in longstanding cases. Patho-morphological studies of early stages indicated that these lipogranulomas arose from stagnant chyle. The composition of fatty acids of a newly formed mesenteric granuloma was determined, together with fatty acids in liver, plasma and the feed. The results supported the pathological observations, as the fat of the granuloma differed from that of the liver and plasma, and contained only small amounts of the endogenous arachidonic acid, while the exogenous eicosenoic acid was present in amounts comparable with the dietary fat. [ABSTRACT FROM AUTHOR]