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At least 19 recordsLinked to original sources
PubMed1977

Analysis of ochratoxin B alone and in the presence of ochratoxin A, using carboxypeptidase A.

A method is described for ochratoxin B analysis, which is adapted to the earlier described method of ochratoxin A analysis, using carboxypeptidase A (K. Hult and S. Gatenbeck, J. Assoc. Off. Anal. Chem. 59:128-129, 1976). The fluorescence spectra of ochratoxins A and B coincide too much to allow direct discrimination of the two compounds. A method using the differences in kinetic parameters of the enzymatic hydrolysis of the two compounds is suggested for the analysis of mixtures of the ochratoxins.

Carboxypeptidases↗
PubMed1976

Production of antibody against ochratoxin A.

Antibody against ochratoxin A was obtained after repeated injection of different protein-ochratoxin A conjugates to rabbits. Among many protein-ochratoxin conjugates tested, bovine serum albumin-ochratoxin A was found to be the best antigen. The antibody is specific for ochratoxins A, C, and T, but is not specific for ochratoxins B, alpha, and other coumarin derivatives. The sensitivity for ochratoxin A detection using a binding assay is in the range of 0.5 to 10 ng/0.5-ml sample. Detailed methods for the preparation of protein-ochratoxin conjugates, preparation of immune serum, and methods for antibody titers are described.

Animals↗
PubMed1979

In vivo and in vitro changes in renal function caused by ochratoxin A in the rat.

Ochratoxin A has been suggested to be an important, environmentally prominent nephrotoxin. Possible involvement in both human and animal disease states has been indicated. This study was designed to examine under controlled laboratory conditions, the nephrotoxic potential of ochratoxin A in the rat. Daily administration of ochratoxin A in doses of 0.75 and 2.0 mg/kg caused persistent urinary hypoosmolality coupled with excessive glucose and protein excretion. In addition the renal slice transport of several organic compounds also was altered. Renal slice tissue electrolytes and water were unaffected by ochratoxin A pretreatment. Direct addition of ochratoxin A to fresh renal cortex slices also depressed transport of some organic compounds. Although rats pretreated with ochratoxin A lost large amounts of body weight, the weight loss alone did not account totally for the changes in renal function. These data indicate that ochratoxin A has the capability of producing alterations in renal function suggestive of nephrotoxicity. However, the pattern of response is different than that observed with citrinin.

Aminobutyrates↗
PubMed1976

Production of ochratoxin A by Aspergillus ochraceus NRRL-3174 before and after exposures to 60Co irradiation.

Spores from the toxigenic organism Aspergillus ochraceus NRRL-3174 were exposed to specific levels of gamma irradiation and then allowed to germinate on selected media. Increases in ochratoxin A production by irradiated, compared to non-irradiated, spores were observed after inoculation of spores onto a cracked red wheat or into a synthetic liquid medium. Variations in daily ochratoxin production were also observed for control and irradiated spore-derived cultures developing on both media, with maximum toxin production varying from 7 to 11 days of incubation. The most notable increases in ochratoxin A production occurred from cultures developing from spores having been irradiated with 10, 25, or 50 krad. Exposures to 400 or 600 krad resulted in complete inhibition of spore germination and, consequently, no ochratoxin production. Of the two substrates used, wheat and synthetic, the quantities of ochratoxin A produced were significantly lower in the synthetic media than on the natural substrate. Higher and more rapid toxin production occurred from spores having been irradiated with 10, 25, 50, and 100 krad than occurred from the non-irradiated control spores when grown on synthetic media. Cultures derived from spores having been exposed to 10, 25, 50, and 100 krad produced significantly higher levels of ochratoxin A after 8 days of incubation on natural substrate than did the controls. Analysis of variance revealed that substrate, length of incubation, as well as irradiation levels all affected the time required to produce maximum levels of ochratoxin A.

Aspergillus↗
PubMed1978

Ochratoxin A as the cause of spontaneous nephropathy in fattening pigs.

At a number of slaughters nephropathy and high ochratoxin A contents in kidneys have been observed in fattening pigs from two Swedish farms. In one herd the source of contamination was barley grown on the home farm and stored under such conditions that the growth of fungal species (Penicillium verrucosum var. verrucosum) producing ochratoxin A occurred, with the subsequent formation of the toxin. In this case high ochratoxin A levels in fattening pigs were found during a period of about 18 months. In the second herd, where compounded feed was used, it was impossible to locate the source of contamination. It was presumed that a consignment of feed was damaged by rain during storage at the farm. Ochratoxin A was found in fattening pigs from this herd for a period of about 2 months. Ochratoxin A appeared in the kidneys of all investigated pigs. In some animals the livers, whole blood, and plasma were analyzed, too. The livers contained somewhat lower amounts of ochratoxin A than the kidneys, whereas the content in whole blood and plasma, respectively, was 5 and 13 times greater. Kidneys spontaneously contaminated with ochratoxin A, when stored for 10 months at -70 degrees C, showed no systematic decrease in toxin content.

Animal Feed↗
PubMed1979

Ochratoxin A in pig blood: method of analysis and use as a tool for feed studies.

A procedure is presented for screening the quality of feed in respect to ochratoxin A contamination based upon the analysis of ochratoxin A in pig blood. Representative samples from large feed lots may be obtained by using pigs as in vivo sample collectors which enrich the toxin and forms homogeneous samples in the blood. The spectrofluorometric procedure for ochratoxin A analysis (K. Hult and S. Gatenbeck, J. Assoc. Off. Anal. Chem. 59:128-129, 1976) has been adapted to pig blood and has been simplified to involve only three extraction steps. A volume of 2.5 ml of blood or plasma is needed, and the detection limit is 2 ng of ochratoxin A per ml. The disappearance of ochratoxin A from pig blood as a function of time has been studied. A feeding experiment with ochratoxin A has been performed, and the time course of the concentration of ochratoxin A in blood has been followed during the experiment.

Animal Feed↗
PubMedDate not supplied

The pharmacokinetic profile of ochratoxin A in the rat after oral and intravenous administration.

A single oral or iv dose (2.5 mg/kg) of ochratoxin A was administered to healthy adult rats. A spectrofluorimetric method was used to determine the toxin level in plasma. The results suggest that the toxin is distributed in two kinetically distinct body compartments. By use of computer techniques, values were assigned to the pharmacokinetic parameters for ochratoxin A in the rat. The half-life of the drug was around 55 hr for either oral or iv administration. Digital computer-simulated curves of the toxin levels in the central and peripheral compartments as well as a total elimination curve were generated. When 14C-ochratoxin A was administered to rats, there were peaks of radioactivity 1 and 6 hr after injection. Ochratoxin alpha was the only metabolite recovered from the cecum and large intestine. Ochratoxin A was excreted via urine and feces, both as the free drug and hydroylzed to ochratoxin alpha; in urine there were five unidentified labeled metabolites. Some of the water-soluble radioactivity was not recovered in the acidic ether extract of the excreta. A hierarchical clustering technique was used to classify the organs in central and peripheral compartments. Muscle, fat, and skin were found to belong to the deep compartment. The residue problem is discussed.

Administration, Oral↗
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↗
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↗
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↗
PubMed1977

Ochratoxin A and citrinin induced nephrosis in Beagle dogs. II. Pathology.

Beagle dogs were given ochratoxin A (0.1 and 0.2 mg/kg) and citrinin (5 and 10 mg/kg) alone and in two dose combinations for 14 days. The gross lesions included focal peritonitis and intestinal intussusceptions in dogs given citrinin. Changes in the kidneys of dogs given ochratoxin A were degeneration and necrosis with desquamation of tubular epithelial cells, primarily in the straight segment of the proximal tubules. Dogs given 10 mg/kg citrin had similar changes in the distal tubules and collecting ducts. Dogs given combined doses of citrinin and ochratoxin A had degeneration and necrosis in proximal and distal tubules, and in thin segments and the collecting ducts; there were desquamated cells and granular casts in the lumina. Dogs given ochratoxin A had necrosis of lymphoid tissues in the spleen, tonsil, thymus, peripheral lymph nodes and lymph nodules of the ileum, colon and rectum. There was ulceration of the mucosa of the intestine in dogs given large combined doses of ochratoxin A and citrinin.

Animals↗
PubMed1979

A leucocytopenia induced in chickens by dietary ochratoxin A.

Ochratoxin A was fed (0, .5, 1.0, 2.0, 4.0, and 8.0 microgram/g) to broiler chickens from day-old to three weeks of age when the birds were bled and total leucocyte and differential counts were performed. Ochratoxin A significantly (P less than .05) reduced leucocyte counts at every dose level of ochratoxin A administered. The leucocytopenia was characterized by an increase in the relative concentration of heterophils and decrease in the relative concentration of lymphocytes. From total leucocyte and differential leucocyte counts the number of circulating cells was calculated for each type of leucocyte. The total number of circulating lymphocytes of blood decreased significantly (P less than .05) at every dose level of ochratoxin A administered, and the number of monocytes decreased at 2.0 microgram/g and above. However, the number of circulating heterophils was not altered. These data demonstrated that ochratoxin A induced a severe leucocytopenia (lympocytopenia primarily and monocytopenia to a lesser extent) and implied that the functioning of the immune system might be altered.

Animals↗
PubMed1979

High pressure liquid chromatographic determination of ochratoxin A and zearalenone in cereals.

A high pressure liquid chromatographic (HPLC) method has been developed for determining ochratoxin A and zearalenone in cereals. The sample is extracted with phosphoric acid and chloroform. The extract is cleaned by washing on a silica gel column with cyclohexane-ethylene dichloride-ethyl ether. After eluting zearalenone with chloroform, ochratoxin A is eluted with chloroform-formic acid. Zearalenone is extracted into alkaline solution, washed with chloroform, the pH is adjusted, and the zearalenone is extracted back into chloroform. Ochratoxin A is purified by chromatography on aqueous sodium biarbonate-Celite. The mycotoxins are determined by using a liquid chromatograph with 2 columns in series packed with Spherisorb ODS 10 micrometer and 5 micrometers, respectively. Ochratoxin A is detected with a speftrophotofluorometer, coupled in series with an ultra-violet detector for estimation of zearalenone. Detection limits are 1-5 micrograms/kg for ochratoxin A and 2 micrograms/kg for zearalenone.

Chromatography, High Pressure Liquid↗
PubMed1978

Effects in mice of simultaneous prenatal exposure to ochratoxin A and T-2 toxin.

Aspergillus ochraceus and Fusarium tricinctum are food contaminating molds whose toxic metabolites, ochratoxin A and T-2 toxin, are known mammalian teratogens. In order to determine the possible effects of simultaneous exposure to such environmental agents, ochratoxin A (2 or 4 mg/kg) and T-2 toxin (0.5 mg/kg) were injected ip, either together or individually, in CD-1 mice on gestation days 8 or 10. Ochratoxin induced craniofacial malformations when given alone on day 8, but not on day 10. T-2 toxin induced tail and limb anomalies particularly when given on day 10. When the two toxins were given together on day 10, ochratoxin exacerbated the incidence of T-2 induced gross malformations. An increase in fetocidal effects was also noted in groups treated at the high dose combination on either day, and effects on fetal growth of the high dose combination given on day 10 were greater than those of the other treatments. Few skeletal or visceral malformations were noted. These results indicated that two teratogens with presumably differing mechanisms of teratogenesis may have additive effects when administered concurrently to the same animal. Such results could be due to generalized toxic effects on the fetus or to more specific mechanisms, but further information is needed to differentiate between the two possibilities.

Abnormalities, Drug-Induced↗
PubMed1978

Studies on the influence of ochratoxin A on rat lenses.

The influence of ochratoxin A on enzyme activities and on the content of free adenine nucleotides and intermediates of glycolysis in rat lenses was investigated. For a period of eight weeks, five times weekly, albino Wistat rats received ochratoxin A in 0.1% NaHCO3, dosed 1/100 LD50, via stomach tube. All measurements were made at the end of the experiment. Decreased contents of ATP, G-6-P, sum of fructose, and F-6-P were observed, but pyruvic acid, AMP, and DAP increased. Relatively decreased activities of enzymes MDH, ALD, HK, GK, and PK were established. The influence of ochratoxin A on the carbohydrate metabolism of rat lenses with respect to tranparency is discussed. There were no significant differences in absolute lens weight in animals treated by ochratoxin A and controls.

Adenosine Diphosphate↗
PubMed1977

Balkan (endemic) nephropathy and foodborn ochratoxin A: preliminary results of a survey of foodstuffs.

Ochratoxin A is a nephrotoxic fungal metabolite (mycotoxin) occurring in foodstuffs. The compound is causally associated with mycotoxic porcine nephropathy, a disease comparable with a human kidney disease, Balkan endemic nephropathy. A preliminary survey of home-produced foodstuffs in areas of Yugoslavia revealed that contamination with ochratoxin A is more frequent in an area where Balkan endemic nephropathy is prevalent (endemic area) than in area where this disease is absent. This indicates higher exposure to foodborn ochratoxin A in the endemic area. Thus further evidence is provided supporting the hypothesis that ochratoxin A is a disease determinant of Balkan endemic nephropathyk0

Food Analysis↗
PubMed1979

Ochratoxin A contamination of foodstuffs in an area with Balkan (endemic) nephropathy.

Ochratoxin A is a nephrotoxic fungal metabolite (mycotoxin) occurring in foodstuffs. The compound is causally associated with mycotoxic porcine nephropathy, a disease comparable with a human kidney disease, Balkan (endemic) nephropathy. A survey of 768 samples of foodstuffs (cereals and bread), locally produced in an area of Yugoslavia where Balkan (endemic) nephropathy is prevalent, has revealed that ochratoxin A is constantly present in parts of foodstuffs. The mean frequency of ochratoxin A contamination of cereals in the study period was 8.7 per cent, but a pronounced annual variation was encountered, with frequencies of contamination up to 43 per cent. These contamination frequencies are higher than those reported elsewhere for foodstuffs for human consumption. Thus further evidence is provided to support the hypothesis that ochratoxin A might by a disease determinant of Balkan (endemic) nephropathy.

Adult↗