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At least 37 records · Page 2Linked to original sources
PubMed1994

The vitamin E nutritional status of rats fed on diets high in fish oil, linseed oil or sunflower seed oil.

Twelve groups of eight rats and two control groups of sixteen rats were given semisynthetic diets with 40% energy as fat for a period of 76 d. All diets contained a minimum of 3% energy as linoleic acid and comparable basal levels of D-alpha- and D-gamma-tocopherol. The diets varied in fat composition and in the content of DL-alpha-tocopheryl acetate. The diets high in polyunsaturated fatty acids (PUFA) were either rich in fish oil (FO; groups 1-4; 10% energy as fish oil PUFA), linseed oil (LN; groups 1-4; 10% energy as alpha-linolenic acid) or sunflower seed oil (SF; groups 1-4; 10 + 3% energy as linoleic acid). The control groups were given a diet high in monounsaturated fatty acids (MUFA; CO 1; 10 + 13% energy as oleic acid) or a diet with an 'average' linoleic acid content (CO 2; 8.5% energy as linoleic acid). Of each high PUFA diet three groups were supplemented with graded levels of DL-alpha-tocopheryl acetate. Steatitis, a sensitive histopathological indicator of vitamin E deficiency in animals fed on diets rich in fatty acids with three or more double bonds, was observed only in the adipose tissue of the FO groups, even in the group with the highest DL-alpha-tocopheryl acetate supplementation. Liver and serum alpha-tocopherol levels were found to be positively correlated and liver and serum gamma-tocopherol levels negatively correlated with dietary DL-alpha-tocopheryl acetate. The groups on the FO diets had significantly reduced liver and serum tocopherol levels in comparison with the groups on the other high-PUFA diets. With the supplementation scheme used for the FO groups the liver alpha-tocopherol levels of both control groups were reached but the serum control levels were not.

Adipose Tissue↗
PubMed1978

Fish oil-induced yellow fat disease in rats. II. Enzyme histochemistry of adipose tissue.

Adipose tissue in various stages of fish oil-induced yellow fat disease in the rat had the same acid phosphatase and 5-nucleotidase activity pattern as similar stages of the disorder in mink and pig. A weak acid phosphatase and 5-nucleotidase activity was seen in interstitial lipofuscin-laden macrophages in "stage M" yellow fat disease without fat cell degeneration. Activity of these macrophagic enzymes increased when there was fat cell degeneration ("stage S" and "stage E" yellow fat disease). This different phosphatase activity in the same cell type may result from phagocytosis of substrates with variable digestibility. Macrophages directly surrounding affected fat cells in steatitis areas ("stage S" and "stage E") had strong acid phosphatase and 5-nucleotidase activity. As in the pig, increased 5-nucleotidase activity was found in affected fat cells, which probably indicates plasma membrane damage. Increased nonspecific esterase activity occurred around affected fat cells. Only a small part of this esterase activity originated from inflammatory cells. This indicates that an increase of esterase activity in degenerating adipose tissue may be an endogeneous process in this tissue.

Acid Phosphatase↗
PubMed2005

Hepatocellular toxicosis associated with the alternate administration of carprofen and meloxicam in a siberian husky.

A 4-year-old female Siberian Husky was diagnosed with pyogranulomatous steatitis at the site of a recurrence of left anal sac rupture (day 1). Carprofen and orbifloxacin were given for 13 days without improvement. A single dose of meloxicam was administered prior to surgical resection of the anal sac, and based on elevated liver enzyme activity, liver supportive therapy was initiated. The dog received carprofen and orbifloxacin orally on the evening of day 14. The dog became anorectic the following morning, and began vomiting. Despite supportive therapy, the dog was unresponsive to treatment and died on day 16. Postmortem examination revealed severe vacuolar change and acute necrosis of hepatocytes consistent with carprofen and meloxicam induced-toxicosis.

Animals↗
PubMed2003

Anemia, myopathy, and pansteatitis in vitamin E-deficient captive marmosets (Callithrix spp.).

Five young adult pet marmosets (Callithrix spp.) were presented with weight loss (5/5); fecal retention (3/5); diarrhea (2/5); impaired locomotion (3/5); anemia (4/4); hypoproteinemia or hypoalbuminemia (3/4); elevations of creatine phosphokinase, lactic dehydrogenase, and alanine aminotransferase (3/4); and renal failure with hypercholesterolemia (2/4). All anemic marmosets had low serum vitamin E levels. The anemia responded to vitamin E and selenium therapy in two marmosets. One of the five marmosets died before presentation, and two others died despite therapy. The two marmosets necropsied had degenerative myopathy, pyogranulomatous pansteatitis, and increased erythrophagocytosis and hemosiderosis. The striated muscle and adipose tissue of both marmosets were negative for coxsackievirus ribonucleic acid by in situ hybridization. These findings suggest that vitamin E deficiency may be involved in the development of anemia, myopathy, and steatitis in callitrichids; however, in some marmosets, underlying diseases such as chronic colitis may have influenced the development of anemia and impaired vitamin E status.

Adipose Tissue↗
PubMed1999

Vitamin E deficiency and pansteatitis in juvenile boat-billed herons (Cochlearius cochlearius).

Steatitis due to vitamin E deficiency occurred in three 10-wk-old boat-billed herons (Cochlearius cochlearius) despite daily placement of a powdered vitamin supplement on the fish that was subsequently washed off by the parents. Physical findings included emaciation, yellow-brown subcutaneous nodules, a firm distended coelom, stomatitis, and yellow-white, submucosal pharyngeal nodules. Clinical pathology revealed heterophilic leukocytosis, anemia, hypoproteinemia, and low plasma alpha (alpha)-tocopherol levels (1.94 microg/ml and 2.14 microg/ml). Two of the chicks died of severe, diffuse pansteatitis and respiratory aspergillosis.

Adipose Tissue↗
PubMed1999

Pansteatitis in a free-ranging red-tailed hawk (Buteo jamaicensis).

A free-ranging juvenile female red-tailed hawk (Buteo jamaicensis) that was unable to fly was admitted to a rehabilitation center and died 1 day later. Hematology and serum chemistry abnormalities included moderate regenerative anemia, elevated creatine kinase, and hyperphosphatemia. Necropsy revealed a generalized steatitis, and histology showed a necrotizing and granulomatous pansteatitis with intralesional pigment compatible with ceroid. There was also moderate diffuse myodegeneration, mild multifocal cardiomyopathy, and mild multifocal hepatic necrosis. These changes and lesions resemble those caused by vitamin E deficiency in mammals and fish-eating birds.

Adipose Tissue↗
PubMed1994

Chylous ascites in cats: nine cases (1978-1993).

Medical records of 9 cats with chylous ascites that underwent exploratory celiotomy were reviewed. In 7 cats, chylous ascites was associated with intra-abdominal neoplasia: 4 cats had an unresectable tumor (hemangiosarcoma, 3 cats; paraganglioma, 1 cat) within the mesenteric root; 2 had malignant lymphoma of the small intestine and mesenteric lymph nodes; and 1 had lymphangiosarcoma of the abdominal wall. In 2 cats, chylous ascites was associated with nonneoplastic diseases: 1 cat had severe biliary cirrhosis and an extrahepatic portosystemic shunt; the other had steatitis caused by vitamin E deficiency. Three cats were euthanatized or died at the time of surgery, and 5 cats were euthanatized within 3 months of surgery. One cat with malignant lymphoma responded well to chemotherapy and lived for 14 months after surgery.

Animals↗
PubMedDate not supplied

Etiologic factors and pathologic alterations in selenium-vitamin E deficiency and excess in animals and humans.

The etiology of selenium-vitamin E (Se-E) deficiency diseases may be complex. Many of the syndromes involve combined deficiency of selenium and vitamin E. Selenium moves into the animal and human food chain from soil and plants, which may contain inadequate amounts of the nutrient in many areas of the world. Vitamin E may be in low concentration in many animal feeds unless supplements are added. Some syndromes, such as steatitis in cats, result from an increased requirement of vitamin E in diets that contain large amounts of polyunsaturated fatty acids, and these diseases will only respond to vitamin E administration. Deficiency syndromes in animals owing to pure Se deficiency are infrequent and have been produced mainly by laboratory studies utilizing extreme deficiency conditions. Other factors that may affect the occurrence of these deficiency diseases are concurrent dietary deficiency of S-containing amino acids, bioavailability of different forms of dietary Se, intake of compounds that antagonize Se (e.g., silver salts), and exposure to various prooxidant substances (e.g., iron compounds, oxygen, ozone, and various drugs).

Animals↗
PubMedDate not supplied

Antioxidant status in a squirrel monkey (Saimiri sciureus) with chronic pancreatitis and degenerative myopathy.

A squirrel monkey (Saimiri sciureus) presented with wasting, vomiting and diarrhoea. Haematology revealed elevation of creatinine phosphokinase, lactic dehydrogenase, alanine aminotransferase, amylase and lipase, together with azotaemia and hypoalbuminaemia. Prominent findings were chronic pancreatitis with acinar and ductal plugs, granulomatous and necrotizing peripancreatic steatitis, degenerative myopathy, testicular atrophy, candidiasis and bacterial necrotizing glossitis. Antioxidant analyses revealed low concentrations of serum vitamin E (and apparently A), hepatic selenium and hair zinc. Pancreatitis may have caused malabsorption and maldigestion, associated with deficiency of multiple antioxidants.

Animals↗