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PubMed1980

Occurrence of ochratoxin- and citrinin-producing fungi on developing Danish barley grain.

The distribution of Aspergillus and Penicillium spp. isolates that produce ochratoxin A (AO) and citrinin was studied on developing barley from diverse locations in Denmark during the 1977 crop year. From 33 test fields, 243 isolates of the two genera were obtained with significant numbers of isolates on the grain at the earliest sampling date (1-2 weeks postanthesis). No specific argronomic factor was linked to the distribution of Aspergillus and Penicillium spp. A taxonomic study of 108 representative isolates of the two genera showed that A. flavus, P. chrysogenum, and P. purpurrescens were the predominant species. An investigation of the toxin-production capability of the identified species showed that seven strains (6.5%) produced OA and a single isolate synthesized citrinin. P. purpurrescens was the dominant OA-producing species with four toxin-positive isolates.

Aspergillus↗
PubMed1991

Citrinin as a possible cause of the pruritus, pyrexia, haemorrhagic syndrome in cattle.

An outbreak of the pruritus, pyrexia, haemorrhagic syndrome affected eight of a herd of 175 cows which was divided into two groups of 115 and 60 according to yield. There was no difference in management between them but citrus pulp pellets were fed only to the larger group in which the eight cows were affected. Silage, which had been made without the use of additives, was also fed to both groups. The citrus pulp was visibly mouldy and contained 30 to 40 parts per billion of citrinin. Signs of the syndrome occurred within three days of the cows starting to ingest the citrus pulp, which was fed for 21 days, and the last case occurred six days after the feeding of citrus pulp ceased. Five calves whose dams had been fed citrus pulp were subsequently born with superior prognathism. In contrast to the eight cows that developed the syndrome only one out of 68 heifers which were fed larger quantities of citrus pulp for 10 days developed mild signs of the syndrome and then recovered, suggesting that older animals may be more susceptible. The clinical signs, gross pathology and histopathology are described and compared with those of previous outbreaks. Mycotoxins, particularly citrinin, were strongly implicated as the cause of this outbreak.

Animal Feed↗
PubMedDate not supplied

Chemical confirmatory tests for ochratoxin A, citrinin, penicillic acid, sterigmatocystin, and zearalenone performed directly on thin layer chromatographic plates.

Published tests have been improved and a new procedure is described for chemical confirmation of mycotoxins directly on thin layer plates. After extraction and preliminary cleanup chromatography with n-hexane or chloroform, the mycotoxins ochratoxin A, citrinin, penicillic acid, sterigmatocystin, and zearalenone were easily separated by thin layer chromatography (TLC) using toluene-ethyl acetate-90% formic acid (6 + 3 + 1) developing solvent. In chemical confirmatory methods, the developed chromatogram was exposed to vapors of pyridine, acetic anhydride, or a mixture, or the mycotoxins were over-spotted. With this treatment, ochratoxin A, citrinin, penicillic acid, and zearalenone were converted to new fluorescent compounds, and observed under 365 nm light after re-chromatography with the same developing solvent. Sterigmatocystin was confirmed chemically using TLC plates impregnated with 0.6N H2SO4 or 10% oxalic acid in methanol. The described procedures are satisfactory for confirming mycotoxins present in standards, artificially contaminated grain samples (barley, corn, oat, rye, and wheat), and extracts from both fungal cultures and naturally contaminated grain samples.

Chemical Phenomena↗
PubMed1983

Rapid thin layer chromatographic determination of patulin, citrinin, and aflatoxin in apples and pears, and their juices and jams.

A method is described to determine the mycotoxins patulin, citrinin, and aflatoxins in apples and pears and their juices and jams. The mycotoxins are extracted with a mixture of acetonitrile and 4% aqueous KC1 (9 + 1). The extract is cleaned up with water and then acidified, and the toxins are recovered with chloroform and separated by thin layer chromatography. Toxin identity is confirmed with various developing solvents, spray reagents, and chemical reactions, and then quantitated by the limit of detection method. The minimum detectable concentrations of the mycotoxins are patulin, 120-130 micrograms/kg; citrinin, 30-40 micrograms/kg; aflatoxin B1 or G1, 2-2.8 micrograms/kg; aflatoxin B2 or G2, 2 micrograms/kg.

Aflatoxins↗
PubMed1993

Experimental citrinin nephrotoxicosis in dogs: renal function evaluation.

To assess renal function changes in acute nephrotoxicosis in dogs, the development and evolution of renal damage during induced citrinin intoxication were studied. Six dogs (experimental group) were given 10 mg citrinin/kg/BW every 24 h during 2 d, and 5 dogs (control group) received exclusively the diluent (1 ml 1% sodium carbonate/kg/BW/d for 2 d). The dogs were daily submitted to physical examination, urinalysis and blood biochemistry analyses (blood urea, serum creatinine, potassium, sodium and glucose) during 2 w. The citrinin-induced renal lesions were mainly in the proximal convoluted tubule and characterized by proteinuria, glucosuria and the presence of numerous granular casts in the urine sediment; these could be detected before elevations in blood urea and creatinine. Glucosuria was the earliest abnormality found and lasted 5 d, while proteinuria and cylindruria were observed from days 1 to 5 and from days 1 to 15, respectively. The glomerular filtration rate was slightly affected as observed by blood urea and creatinine elevations from days 2 to 5. Urine analysis is a useful tool for the evaluation of nephrotoxicity since most nephrotoxins act primarily on the proximal convoluted tubule.

Animals↗
PubMed1977

Time-dependent, irreversible inhibition of 3-hydroxy-3-methylglutaryl-coenzyme A reductase by the antibiotic citrinin.

The inhibition of 3-hydroxy-3-methylglutaryl-CoA reductase by citrinin, an antibiotic, has been studied. The inhibition was the mixed type with respect to 3-hydroxy-3-methylglutaryl-CoA and non-competitive with respect to NADPH. When the enzyme was preincubated with citrinin prior to enzyme assay, however, it caused a time-dependent, irreversible inhibition, possibly by binding to a site distinct from the active center on the enzyme protein.

Alcohol Oxidoreductases↗
PubMed1999

Biosynthetic pathway of citrinin in the filamentous fungus monascus ruber as revealed by 13C nuclear magnetic resonance

Carbon isotope distribution of [13C]citrinin from Monascus ruber incubated with [13C]acetate revealed that the biosynthesis of the toxin originated from a tetraketide, instead of a pentaketide as has been shown for Penicillium and Aspergillus species. The production of polyketide red pigments and citrinin by M. ruber may therefore be regulated at the level of the tetraketide branch point.

Journal Article↗
PubMed1974

Fate of ochratoxin A and citrinin during malting and brewing experiments.

The fate of ochratoxin A and citrinin during malting and brewing processes was studied by the use of naturally contaminated lots of barley, as well as by the addition of crystalline toxins to the mash. Complete degradation was observed for ochratoxin A from moderately contaminated barley lots and for citrinin added to mash. The use of highly contaminated barley resulted in transmission of ochratoxin A into the beer, but only 2 to 7% of the initial content was detected, corresponding to levels of 6 to 20 mug of ochratoxin A per liter of beer. Barley lots with this high ochratoxin contamination (1,000 to 5,000 mug/kg) will be easily detected and, therefore, because of pronounced deterioration, should be rejected during inspection upon admittance to the breweries.

Amylases↗
PubMedDate not supplied

Citrinin and endosulfan induced teratogenic effects in Wistar rats.

Dietary exposures to food pollutants such as mycotoxin(s) or pesticide(s) are most significant due to their adverse effects on the production and reproduction in animals and the human population. The present investigation was conducted to evaluate the teratogenic potential of citrinin (CIT) and endosulfan either alone or in combination in pregnant rats during gestational days 6-20. Endosulfan (1 mg kg(-1) body weight, by oral intubation) and CIT (10 mg kg(-1) feed, through diet) when administered either alone or in combination in pregnant rats caused significant teratogenic effects in the developing fetuses. There was no maternal mortality, however, reduced maternal weight gain and number of live fetuses and increased fetal resorptions were recorded in all the treated groups. The fetal body weights and crown to rump lengths were significantly decreased and the per cent gross, visceral and skeletal anomalies were significantly increased in the fetuses of dams of all the treated groups. The internal hydrocephalus, cerebellar hypoplasia, microphthalmia, contracted and notched kidneys, multilobulated liver, dilated renal pelvis, incomplete ossification of skull bones, rib anomalies and sacral and caudal vertebrae agenesis were the important fetal malformations. The occurrence of fetal gross, skeletal and visceral malformations was more severe in the combination group, suggesting an additive interaction of CIT and endosulfan in inducing developmental toxicity in Wistar rats.

Abnormalities, Drug-Induced↗
PubMed2006

Preliminary data on the presence of mycotoxins (ochratoxin A, citrinin and aflatoxin B1) in black table olives "Greek style" of Moroccan origin.

Many mould strains, in particular Aspergillus and/or Penicillium, are able to develop on olive and produce ochratoxin A (OTA) and/or citrinin (CIT) and/or aflatoxin B (AFB) after harvest, during drying and storage of olives. The development of fungi on olives is responsible for the reduction of nutritional quality of olive because they can disturb the synthesis of the fatty acids. OTA, CIT and AFB are particularly dangerous for health, inducing cancer of urinary tracts or liver carcinoma. In this study, ten olive samples bought at retailer and at supermarket in Morocco were analyzed for their OTA, CIT and AFB contents. These three mycotoxins were extracted simultaneously by a method based on solvent partition validated in-house, then separated by HPLC coupled to a fluorescence detector. All olive samples contain OTA ranging from LOQ to 1.02 microg/kg. Respectively, 50 and 25% from retailer and supermarket samples were contaminated by more than 0.65 microg/kg. In addition, 80% of olive samples contained CIT above LOD, and 100% of olive tested contained AFB above 0.5 microg/kg. As simultaneous presence of these toxins increases toxic risks, it is thus essential to have a good control of the conservation of olives after harvest.

Aflatoxin B1↗
PubMed2004

The effects of the Penicillium mycotoxins citrinin, cyclopiazonic acid, ochratoxin A, patulin, penicillic acid, and roquefortine C on in vitro proliferation of porcine lymphocytes.

The in vitro effect of each of the Penicillium mycotoxins citrinin (CIT), cyclopiazonic acid (CPA), ochratoxin A (OTA), patulin (PAT), penicillic acid (PIA) and roquefortine C (RQC) on mitogen induced lymphocyte proliferation was determined using purified lymphocytes from 6 piglets. Dose response curves for each mycotoxin were generated and the concentrations producing 50% inhibition of cell proliferation (IC(50)) were estimated. OTA and PAT were the most potent toxins with IC(50) of 1.3 and 1.2 micromol/l, respectively (0.52 and 0.18 mg/l, respectively). Based on molar concentrations, OTA was 15, 30, 40, and 65 times more potent as an inhibitor than PIA, CIT, CPA and RQC, respectively.

Animals↗
PubMed2007

Ochratoxin A and citrinin nephrotoxicity in New Zealand White rabbits: an ultrastructural assessment.

In the present investigation, ochratoxin A (OTA) (0.75 mg/kg feed) and citrinin (CIT) (15 mg/kg feed) were fed alone and in combination to young growing New Zealand White rabbits for 60 days to evaluate renal ultrastructural alterations. The severity and intensity of renal ultrastructural changes varied with the type of the treatment, and predominant and consistent lesions were recorded in the proximal convoluted tubule (PCT) lining cells. The significant changes in mitochondria, the most affected cell organelle in all the treatment groups, included mitochondrial disintegration and distortion, pleomorphism, cluster formation and misshapen appearance such as signet ring, dumbbell, cup and U shapes. Intra-cisternal sequestrations of involuting mitochondria, and thickening of basal layer of PCT epithelial cells with partial detachment, were the characteristic features observed in OTA and combination treatments. CIT treatment revealed crenated nucleus, loss of nucleolus, depletion of cytoplasmic organelles, mitochondrial pleomorphism, nuclear fragmentation, uniform folding of cell membrane and cytoplasmic vacuolations in the PCTs. Focal thickening of the glomerular basement membrane and degeneration of endothelial cells were the prominent alterations in the glomeruli in OTA and combination treatments. Distal convoluted tubules were unaffected in CIT treatment, however, mild to moderate lesions were observed in OTA and combination treated rabbits. It may be concluded that on simultaneous exposure, CIT potentiated the toxic effects of OTA on renal ultrastructure.

Animal Feed↗
PubMed1991

The role of altered mitochondrial function in citrinin-induced toxicity to rat renal proximal tubule suspensions.

Citrinin (CTN), a mycotoxin produced by several species of Penicillium and Aspergillus, causes renal proximal tubule (RPT) cell injury and death by an unknown mechanism of action. Using suspensions of rat RPT, the cellular events preceding CTN-induced cytotoxicity were investigated. Tubule viability decreased in a concentration- and time-dependent manner after CTN exposure, with cell death beginning 1, 2, and 4 hr after exposure to 500, 125-250, and 63 microM, respectively. Basal oxygen consumption (QO2) of RPT increased from 41 to 53 nmol O2.mg protein-1.min-1 30 min after exposure to 250 microM CTN and returned to control values 1 hr after exposure. A similar concentration- and time-dependent transitory rise in basal QO2 occurred at all concentrations of CTN tested (63-500 microM). Nystatin-stimulated QO2, an indirect measure of mitochondrial state 3 respiration in RPT, decreased 11% at 0.5 and 1 hr after exposure to 500 and 250 microM CTN, respectively, but was not affected after exposure to 63 and 125 microM CTN. Adenosine triphosphate content declined 22% to 48% in RPT at 0.5 and 1.5 hr after exposure to 500 and 125-250 microM CTN, respectively. Although lipid peroxidation occurred concurrently with RPT cell death, iron-mediated oxidative stress was not a causative factor in the development of toxicity since pretreatment with 1 mM deferoxamine prevented iron-mediated lipid peroxidation but did not protect RPT from CTN-induced cell death. Further studies using RPT and isolated renal cortical mitochondria (RCM) showed that CTN had multiple effects on mitochondrial function. Direct probing of mitochondrial function within RPT showed that a 1-hr exposure to 250 microM CTN increased spontaneous respiration 55% in RPT respiring on the site I respiratory substrates glutamate/malate while state 3 respiration decreased 34%. CTN also decreased succinate supported respiration but had no effect on cytochrome c-cytochrome oxidase. With isolated RCM, a 3-min exposure to 125 and 250 microM CTN increased state 4 respiration in the absence of a phosphate acceptor 27 and 67%, respectively, while 250 microM CTN decreased state 3 respiration 23%. Respiration in the presence of a known uncoupler was reduced after CTN exposure (63-250 microM) in a concentration-dependent manner. These results indicate that CTN has multiple effects on mitochondrial function in RPT and isolated RCM which may contribute to the development of cell death in rat RPT.

Animals↗
PubMed1984

Citrinin mycotoxicosis in the rabbit: clinicopathological alterations.

Citrinin, a nephrotoxic mycotoxin, was dissolved in 0.5 N-NaOH neutralized with HCl and given in a single oral dose of 120 mg/kg (Trial I) or 80 or 100 mg/kg (Trial II) to male New Zealand white rabbits weighing 2.0-2.7 kg. In Trial I, sequential measurements of clinicopathological parameters were made over a 24-hr period. Azotaemia and metabolic acidosis with haemoconcentration and hypokalaemia developed within 4-12 hr. In Trial II, clinicopathological and urinary parameters were measured daily for 7 days. Increased blood urea nitrogen and serum-creatine levels and decreased creatinine clearance indicated renal failure; these values were most abnormal on days 2-4, returning to normal or near normal by day 7 in rabbits that survived. Urine analysis indicated tubular dysfunction and necrosis with glucosuria, isosthenuria and cylindruria; most urinary parameters were normal by day 7.

Animals↗
PubMed2005

Citrinin induces apoptosis in HL-60 cells via activation of the mitochondrial pathway.

The mycotoxin citrinin (CTN), a frequent natural contaminants of certain food and feeds, is known to be cytotoxic and genotoxic to various mammalian cells. To investigate the death mode of cells exposed to CTN, human promyelocytic leukemia (HL-60) cells were chosen to identify the apoptotic process induced by CTN. Morphological evidence of apoptosis, including nuclei fragmentation and DNA laddering formation, was clearly observed 24h after exposure to CTN. Flow cytometry analysis revealed that apoptotic cells in the hypodiploid region dramatically increased in cultures treated with CTN at concentrations above 50muM. Results of Western blotting showed that CTN induced the formation of processed caspase-3, -6, -7, -9, but not caspase-8, in a dose-dependent manner; CTN also induced a time-dependent increase in caspase-3 catalytic activity. The apoptosis triggered by CTN in HL-60 was accompanied by the cytochrome c release from mitochondria to cytoplasm. The presence of antioxidants in cultures did not effectively suppress CTN-induced cytotoxicity and caspase-3 activity. These findings suggest that CTN induces apoptosis in HL-60 cells by stimulating cytochrome c release followed by activation of multiple caspases, but oxidative stress may not play a role in the apoptotic process.

Antioxidants↗
PubMed1999

Reversed-phase liquid chromatographic behavior of the mycotoxins citrinin and ochratoxin A.

The reversed-phase (RP) chromatographic behavior of citrinin (CT) and ochratoxin A (OA), the latter introduced as reference substance, were studied as a function of hydrophobicity and silanophilic activities of the stationary phase, pH, type of acid in the eluent, its composition as well as of the column temperature. While OA's affinity to RP materials was not influenced by phase material properties, CT showed a high affinity to hydrophobic phase materials, and its elution order, compared to OA, depended strongly on the phase material chosen. In practice, all octadecyl stationary phases under investigation allowed proper conditions for CT and OA chromatography if judicious selection of influencing parameters, especially a low pH and applying an acid with a pKa<2.3, were chosen.

Acids↗