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Biomedical subjects

F Elling

Publications and source records attributed to F Elling.

14 recordsLinked to original sources
PubMed1979

Tissue distribution of radioactivity from ochratoxin A-14C in rats.

Examination of the distribution of radioactivity in rat tissues during the first 24 hr after administration of ochratoxin A-14C demonstrated maximum accumulation in stomach and kidney. The highest counts were observed in stomach, lung, kidney, thymus, spleen and heart during the first 6 hr after treatment, whereas the brain, liver muscle, duodenum, jejunum, ileum, and cecum exhibited the greatest counts at 18 hr after toxin exposure.

Animals↗
PubMed1979

Ochratoxin A-induced mycotoxic porcine nephropathy: alterations in enzyme activity in tubular cells.

Mycotoxic porcine nephropathy was induced by p.o. administration of crystalline ochratoxin A for periods of 5 days, 3 months and 2 years. Enzyme activities of the renal tissue were studied histochemically. These were NADH-tetrazolium reductase, NADPH-tetrazolium reductase, lactate dehydrogenase, isocitrate dehydrogenase, succinate dehydrogenase, glucose-6-phosphate dehydrogenase, alpha-glycerophosphate dehydrogenase, unspecific acid phosphatase and unspecific alkaline phosphatase. The activity of NADH-tetrazolium reductase and succinate dehydrogenase was reduced in the proximal tubule of all nephrons after 5 days ochratoxin A exposure and remained reduced after 3 months and 2 years exposure. The effect of ochratoxin A on these enzymes would appear to cause the impairment of proximal tubular function and the morphological changes observed in the proximal tubule in ochratoxin A-induced mycotoxic porcine nephropathy. The localization of alterations in enzyme activity corresponds to the localization of ochratoxin A previously demonstrated in the kidney. The activities of NADPH-tetrazolium reductase, lactate dehydrogenase, glucose-6-phosphate dehydrogenase and unspecific alkaline phosphatase were reduced focally corresponding to the areas with focal tubular atrophy and the degree of reduction was roughly parallel to the degree of atrophy.

Acid Phosphatase↗
PubMed1979

Nutritionally induced necrotizing glomerulonephritis and polyarteritis nodosa in pigs.

A florid necrotizing glomerulonephritis was found in all 48 pigs that were fed a waste product from the industrial production of the proteolytic enzyme Alcalase NOVO. In addition, three of the animals developed a lesion identical to polyarteritis nodosa. Focal necrosis of the glomeruli was observed in all animals. Electron microscopy showed electron dense deposits at the subendothelial and subepithelial side of the basement membrane of the glomerular capillary wall and in the mesangium. Immunofluorescence microscopy showed IgM in a fine granular pattern in the glomeruli of all 48 pigs. This appears to be the first report on nutritionally induced glomerulonephritis and polyarteritis nodosa in pigs.

Animal Feed↗
PubMed1979

Porcine nephropathy induced by long-term ingestion of ochratoxin A.

Nine pigs were fed crystalline ochratoxin A in their feed at a concentration of about 1 mg/kg. Three pigs and their controls were killed after 3 months and 6 pigs and controls were killed after 2 years. A decrease of the ratio TmPAH/CIn, increased urinary glucose excretion and decreased ability to concentrate urine, occurred within a few weeks and aggravated slightly during the 2-year period. Changes in renal structure, characterized by degeneration and atrophy of proximal tubules, interstitial fibrosis and hyalinization of glomeruli, were progressive during time of exposure, but terminal renal failure was not reached. The kidney, liver, muscular and adipose tissue contained 3 to 27 microgram ochratoxin A/kg after 3 months of exposure. No further accumulation of ochratoxin A residue was found after 2 years of exposure.

Animals↗
PubMed1978

Structural changes in kidneys of patients with oliguric extracapillary glomerulonephritis during immunosuppressive therapy.

Structural changes in kidney biopsies were investigated from five patients with primary oliguric extracapillary glomerulonephritis in whom the renal function was adequately maintained during extended combined immunosuppressive treatment. The most important structural change was a pronounced decrease in the number of crescents. Reduction in numbers of crescents in the late biopsies was significantly greater than the increase in the number of hyalinized glomeruli. Tubular parenchyma showed only slight diffuse atrophy, and a moderate interstitial fibrosis was always present during the latter stages of treatment. Disappearance of crescents in the glomeruli was not accompanied by disappearance of immunoglobulins. Successfull immunosuppressive treatment of extracapillary glomerulonephritis causes the disappearance of structural characteristics of the kidney that are diagnostic for this disease.

Adult↗
PubMed1977

Demonstration of ochratoxin A in kidneys of pigs and rats by immunofluorescence microscopy.

Ochratoxin A was localized in the kidney of pigs and rats by means of immunofluorescence microscopy after short-time exposure. Antibody against ochratoxin A was obtained from rabbits after repeated injections of bovine serum albumin-ochratoxin A conjugate. Ochratoxin A was localized exclusively in the proximal tubule. Light microscopically, necrosis and desquamation of epithelial cells in the pig kidneys were restricted to the proximal tubule where the toxin was found. The investigation had demonstrated conclusively that the proximal tubule is the target part of the nephron in ochratoxin A-induced mycotoxic nephropathy.

Animals↗
PubMed1977

Perfusion fixation of kidneys in adult pigs for electron microscopy.

In five female pigs, weighing approximately 100 kg, laparotomy was made under surgical anesthesia. One kidney was removed for immersion fixation and enzyme histochemistry, while the other kidney was fixed by vascular perfusion without prior interruption of the blood flow. A step-by-step description is given of the perfusion procedure, which requires three assistant. Prior to perfusion, heparin was given in order to prevent intravascular coagulation. 1% glutaraldehyde in Tyrode's solution was used as perfusion fluid. Polyvinylpyrrolidone 2.5% was added in order to adjust the colloid osmotic pressure of the perfusion fluid to that of the blood. Perfusion was maintained for 5 min. The tubules appeared with open lumina, and the proximal tubular cells had evenly arranged brush borders and both lateral and intercellular spaces were narrow and of constant width.

Animals↗
PubMed1976

Experimental avian nephropathy. Changes of renal function and structure induced by ochratoxin A-contaminated feed.

One-day-old chickens were fed ochratoxin A-contaminated diets at 2 levels: 0.3 and 1 mg ochratoxin A per kg feed, for 341 days. The only observable lesion to develop was a kidney damage comparable with the naturally occurring avian nephropathy. The changes in renal function were characterized by impairment of glomerular and tubular function, indicated by a decreased inulin clearance, TmPAH and decreased urine concentrating capacity. The changes of renal structure included degeneration of the tubular epithelium accompanied by regeneration. At slaughter, the kidneys, liver and muscular tissue of the birds contained residues of ochratoxin A (up to 50 mug per kg). As all the birds would have passed the meat inspection because no macroscopical lesions were present, this represents a possible health problem.

Animal Feed↗
PubMed1976

Experimental porcine nephropathy: changes of renal function and structure perorally induced by crystalline ochratoxin A.

Nine pigs were fed crystalline ochratoxin A in amounts corresponding to a feed level of 1 mg per kg for 3 months. The only observable lesion developed was a kidney damage, identical to the naturally occurring porcine nephropathy. The changes of renal function was characterized by impairment of proximal tubular function, indicated by a decrease of the ratio TmPAH/CIn, of the ability to concentrate urine, and by an increased urinary excretion of glucose. The decrease of the ratio TmPAH/CIn is correlated with time of exposure to ochratoxin A. The changes of renal structure were characterized by degeneration of the proximal tubules, leading to tubular atrophy accompanied by interstitial fibrosis. At the end of the experiment the kidney, liver, adipose and muscular tissue of the slaughtered pigs contained sizable amounts of ochratoxin A residues. As the pigs would have passed the meat inspection this represents a possible health problem. The changes observed in this study are identical to those observed by feeding to pigs grains naturally contaminated with ochratoxin A.

Adipose Tissue↗
PubMed1975

Spontaneous toxic nephropathy in poultry associated with ochratoxin A.

At a poultry slaughterhouse 14 birds with macroscopic renal changes were collected, and the kidneys were examined histologically and the muscular tissue was analysed for ochratoxin A residues. Out of 14 birds 5 birds had ochratoxin A residues ranging from 4.3 to 29.2 mug/kg. In 4 of these birds a toxic nephropathy was found characterised by atrophy and degeneration of proximal and distal tubules and interstitial fibrosis. The possibility of birds with ochratoxin A residues being presented for human consumption is discussed.

Animals↗
PubMedDate not supplied

Time-dependent disappearance of ochratoxin A residues in tissues of bacon pigs.

Crystalline ochratoxin A was administered to bacon pigs for one month. After termination of toxin exposure the pigs were slaughtered at different intervals and analyses for ochratoxin A residues in four tissues were conducted. Kidneys contained the highest concentrations, and fat the lowest, at each interval. Ochratoxin A disappeared from muscles and fat after 2 weeks, from liver after 3 weeks, and from the kidneys after 4 weeks. The toxin disappeared from tissues exponentially. All the pigs would have passed the meat inspection because no pathologic lesions were developed although tissues contained mycotoxin residues. The results of this study indicate that contamination of meat by ochratoxin A may be avoided by feeding pigs ochratoxin-free feed during the last 4 weeks before slaughter.

Animals↗