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PubMed1988

Temperature influence on Penicillium citrinum thom growth and citrinin accumulation kinetics.

To study the temperature influence on both Penicillium citrinum growth and citrinin accumulation, a 20, 25 and 30 degrees C. Radial and 30 degrees C. Radial growth rate and lag phase were determined from the increase in colony diameter with time. The optimal temperature for P. citrinum growth was 30 degrees C. Citrinin extracted from the agar medium was determined by thin layer chromatography. Citrinin accumulation kinetics were analyzed by fitting the data to curves generated by using a logistic function. The parameters obtained from this equation demonstrated, for all temperatures studied, that the maximum citrinin accumulation by P. citrinum on Czapek agar with maize extract was at about 30 degrees C. At 37 degrees C a rapid decrease in the citrinin concentration was observed after a maximal value was reached.

Agar↗
PubMed1993

Citrinin-producing capacity of Penicillium expansum strains from apple packinghouses of Lerida (Spain).

A study of the citrinin producing capacity in 122 Penicillium expansum strains isolated from apples and various locations of apple packaging premises Lleida (Spain) was conducted. Among the strains examined, 46% produced citrinin in a laboratory substrate and 73.2% of these strains were isolated from decayed apples. All citrinin producing strains produced metabolites which inhibited Bacillus cereus and Bacillus subtilis. The majority of the strains producing citrinin in solid substrate also produced citrinin in apples and apple juices.

Citrinin↗
PubMed2000

Co-occurrence of ochratoxin A and citrinin in cereals from Bulgarian villages with a history of Balkan endemic nephropathy.

Cereal samples were collected in 1998 from Bulgarian villages without [control village (C), n = 20] or with [endemic villages (E); E1, n = 21; E2, n = 30; E3, n = 23] a history of Balkan endemic nephropathy (BEN). Sampling included foods (wheat, corn) and feeds (barley, oats, wheat bran). Analysis of ochratoxin A and citrinin was done by enzyme immunoassays (EIA), with detection limits of 0.5 and 5 ng/g, respectively. Ochratoxin A-positive results were confirmed by HPLC after immunoaffinity chromatography. Highest toxin levels were found in wheat, wheat bran, and oats. For ochratoxin A, the percentages of positives were 35% (C), 29% (E1), 30% (E2), and 47% (E3), the mean/median values of positives were 1.5/1.3 ng/g (C), 11/1.6 ng/g (E1), 18/1.6 ng/g (E2), and 3.5/1.5 ng/g (E3). For citrinin, 5.0% (C), 14% (E1), 3.3% (E2), and 13% (E3) were positive, and the mean/median values were 6.1/6.1 ng/g (C), 180/83 ng/g (E1), 10/10 ng/g (E2), and 84/20 ng/g (E3). Highest concentrations of ochratoxin (maximum = 140 ng/g) and citrinin (maximum = 420 ng/g) were found in samples from endemic villages. Co-contamination with ochratoxin A and citrinin was found for one sample (14% of positives) from village C and for six samples (22% of positives) from villages E1-E3. Citrinin levels in these samples were 2-200 times higher than those of ochratoxin A.

Animal Feed↗
PubMed2006

Citrinin revisited: from monomers to dimers and beyond.

Detailed chemical analysis of the solid phase fermentation of an Australian Penicillium citrinum isolate has returned the known compounds citrinin (1), phenol A acid (6), dihydrocitrinone (7) and dihydrocitrinin (8), together with a novel cytotoxic dimer, dicitrinin A (5). Dicitrinin A (5) was determined to be a dimerised artefact of the major co-metabolite citrinin, and its structure solved by spectroscopic analysis and chemical modification. Analysis of the products encountered during the controlled decomposition of citrinin led to the discovery of additional citrinin dimers and delineated a plausible mechanistic pathway linking all monomeric and dimeric citrinin degradation products.

Benzofurans↗
PubMed1997

Rapid semi-quantitative fluorimetric determination of citrinin in fungal cultures isolated from cheese and cheese factories.

A new rapid semi-quantitative fluorimetric assay for citrinin production testing in mould cultures has been developed. The chemical structure of the citrinin makes it a weak native fluorophore. This fluorescence can be strongly enhanced in an acidic environment. A standard curve where the concentration of HCl needed to show the yellow fluorescence signal of different concentrations of citrinin was established, thus providing a semi-quantitative method to prove the capacity of toxin production of fungal cultures. Two Penicillium strains from the Spanish National Collection of Type Cultures, were studied for the toxin production on YES broth at 25 degrees C for 21 d. The culture was assayed daily for the presence/absence and quantification of citrinin by adding the HCl concentration set, and also quantified by RP-HPLC as a confirmation procedure. Experiments demonstrate that 5 d are necessary to show the presence of citrinin. As an illustration, a total of 48 strains of Penicillium isolated from cheese and cheese factories were analysed with the proposed method.

Cheese↗
PubMed1977

The mechanism of action of citrinin on rabbit kidney alkaline phosphatase activity in vivo.

The effect of citrinin poisoning on rabbit kidney alkaline phosphatase was investigated. After seven days administration of citrinin (2 mg/kg body weight daily) the animals were sacrificed and the level of enzymes estimated in serum and kidney. Serum enzymes showed no variation in activity in the citrinin-treated animals, but in kidney, alkaline phosphatase activity decreased significantly. The decreased activity was mainly associated with the cytoplasmic fraction and in fractions Ib and II. The enzyme II obtained from citrinin-treated animal showed no kinetic difference in substrate specificity, inhibition by phenylalanine, phosphate, sodium-EDTA and Zn2+ ions, activation by Mg2+ ions, thermal inactivation and electrophoretic mobility to that of control Enzyme II. Immunological studies showed that the decrease in enzyme activity was due to existence of inactive enzyme protein. Hormones like cyclic AMP, prostaglandin E1 and parathyroid hormone reversed the decreased enzyme activity due to citrinin poisoning in mouse and rabbit. This study favours the possible existence of active and inactive forms of alkaline phosphatase in the system.

Alkaline Phosphatase↗
PubMed2005

The mycotoxins citrinin and gliotoxin differentially affect production of the pro-inflammatory cytokines tumour necrosis factor-alpha and interleukin-6, and the anti-inflammatory cytokine interleukin-10.

BACKGROUND: Microbial growth is considered one of the major causes of indoor air problems. Moulds have been associated with asthma, allergy and a wide range of diffuse indoor air-related symptoms. However, mechanisms of the adverse health effects are not well understood. OBJECTIVE: We hypothesized that the mycotoxins citrinin and gliotoxin could cause an imbalance between the secretion of the pro-inflammatory cytokines TNF-alpha and IL-6 and the anti-inflammatory cytokine IL-10. METHODS: We investigated the influence of citrinin and gliotoxin on the human monocytic cell line Mono-Mac-6 (MM6) with and without lipopolysaccharide -stimulation. The levels of IL-10, IL-6 and TNF-alpha were analysed in cell culture supernatants by ELISA. Cell viability and cell apoptosis were measured by flow cytometry. RESULTS: The strongest inhibition of cytokine secretion was found for IL-10. IL-6 levels were found to decrease in a dose-dependent manner along with reduced cell viability. TNF-alpha levels increased with low gliotoxin exposure (less than 100 ng/mL), but decreased significantly at 375 ng/mL and higher along with increased cell apoptosis and reduced cell viability. TNF-alpha levels were not reduced by citrinin exposure. CONCLUSION: We observed a cytokine imbalance with a more pronounced reduction of IL-10 concentrations compared with those of TNF-alpha and IL-6. We suggest that low exposure doses of citrinin and gliotoxin (corresponding to less than 100 ng/mL gliotoxin and less than 10 mug/mL citrinin) may inhibit IL-10 and lead to increased risk of an inflammatory response with relative overproduction of TNF-alpha and IL-6. The findings and their clinical implications must be verified by human studies. However, we speculate that the observed biological effects may be of importance as they may partly explain the occurrence of diffuse general indoor air-related symptoms as well as the worsening of asthmatic inflammatory reactions experienced in mouldy environments.

Air Pollution, Indoor↗
PubMed1977

Ochratoxin A and citrinin induced nephrosis in Beagle dogs. I. Clinical and clinicopathological features.

Ochratoxin A and citrinin, both mycotoxins, were given separately and combined to young Beagle dogs for 14 days. Ochratoxin A, 0.1 and 0.2 mg/kg, was given by capsule, and citrinin, 5 and 10 mg/kg, was dissolved in ethanol and given by intraperitoneal injection. Clinical signs of toxicosis in dogs given 10 mg/kg citrinin and the higher combined doses included anorexia, retching, tenesmus, weight loss, prostration and death. Severity of the clinical disease and mortality were increased when the mycotoxins were combined, which indicated synergism. The clinicopathological abnormalities reflected renal damage, in that glutamic oxaloacetic transaminase and lactic dehydrogenase increased in the urine of the dogs with clinical signs of poisoning. Serum lactic dehydrogenase was increased in dogs given 10 mg/kg citrinin. Cellular and granular casts, ketones, protein and glucose were in the urine of dogs given large doses of citrinin alone or combined with ochratoxin A. Serum concentrations of sodium, potassium and chloride in the dogs given high doses of each group.

Animals↗
PubMed1977

Ochratoxin A and citrinin induced nephrosis in Beagle dogs. III. Terminal renal ultrastructural alterations.

The extent and type of renal ultrastructural changes in Beagle dogs varied with the administration of ochratoxin A and citrinin alone and in the two dosage combinations. The three predominant changes were cytoplasmic vacuolation, myelin figure formation and lesions designated as cytoplasmic disarray. These changes were mainly of the endomembane system of the tubular epithelial cells. Cytoplasmic vacuoles were within proximal and distal tubules and collecting ducts and were most numerous in dogs given 10 mg/kg critrinin. Vacuolation of similar distribution, but less severe, was seen in renal tubular cells of dogs given the higher dose of the combined mycotoxins (0.2 mg/kg ochratoxin A + 10 mg/kg citrinin). This damage was limited to the proximal tubular cells in dogs given only ochratoxin A (0.1 or 0.2 mg/kg). Myelin figures were in proximal epithelial cells of dogs given ochratoxin A alone or combined with citrinin. There was cytoplasmic disarray in dogs of all groups except for dogs given 5 mg/kg citrinin. This lesions was usually limited to the proximal tubules. The lesions, however, was found in cells of the distal tubules of dogs given 10 mg/kg citrinin alone.

Animals↗
PubMed1981

Citrinin toxicity in growing chicks.

Male broiler chicks, from day-old to 3 weeks of age, were fed diets containing 0, 100, 220, 330, and 440 ppm citrinin produced by Penicillium lanosum grown on whole corn. Body weight decreased (P less than .05) when chicks were fed the diets containing 330 and 440 ppm citrinin. Average body weight of chicks fed the diet containing 220 ppm citrinin was 8% less than that of chicks fed no toxin. Feed utilization decreased (P less than .05) with chicks fed the diet containing 440 ppm citrinin. Analysis of thigh muscle, kidney, liver, and blood for citrinin revealed detectable amounts in the liver and blood of chicks fed 440 ppm.

Animals↗
PubMed1985

The effect of drying method and storage time on citrinin activity in corn.

Sterilized whole corn was inoculated with a Penicillium spp.,3 a citrinin-producing fungus, and incubated at room temperature for 8 weeks. The corn was then blended and divided into two parts, which were dried either in air at room temperature (ADC) or in a forced draft oven at 60 C for 24 hr (ODC). Each batch of corn was ground and stored in plastic containers. The corn was fed to broiler chicks prior to and after 3, 6, 9, and 12 months of storage at 4 C. The inoculated corn was fed undiluted or blended with noninoculated corn to give mixtures containing one-third and two-thirds of inoculated corn. Noninoculated corn, inoculated corn, and blends of the two were fed to chicks for 5 hr as the only feed. Feed consumption, water intake, and excretion were measured at the end of the test. The citrinin contents of the ADC at 3, 6, 9, and 12 mo were 824, 599, 667, and 590 ppm and were 928, 541, 781, and 490 ppm for the ODC at the same periods. Water consumption and water excretion increased as the amount of citrinin intake increased. Neither drying method nor length of storage affected the citrinin activity in the corn. The citrinin in ODC was neither bound nor converted to a derivative that was unextractable.

Animal Feed↗
PubMed1988

Effects of ochratoxin A alone and in combination with citrinin on kidney function of single comb White Leghorn pullets.

The present study was designed to evaluate the acute effects of ochratoxin A (OA) on pullet renal function, and to determine if the diuretic effects of citrinin are altered by acute ochratoxicosis. Birds were injected intramuscularly with a 1-mg/mL solution of OA at a dose of 5 mg/kg body weight for 2 consecutive days. Control birds received an equal volume injection of the OA carrier vehicle (100% ethanol). On the 3rd day, birds were anesthetized and prepared for renal function studies. Following 30 min of control urine and plasma collection, an intravenous infusion containing 400 ppm citrinin was initiated, and urine and plasma were collected for an additional 70 min. The OA alone caused an increase in manure moisture and increased hematocrits (hemoconcentration), but direct effects on glomerular filtration rate (GFR), urine flow rate/GFR, para-aminohippuric acid clearance (CPAH), free water clearance (FWC), and electrolye excretion (Na, K, Ca, P) were not consistently demonstrated. The OA may cause hemoconcentration by causing a subtle increase in urine flow (diuresis), or by increasing intestinal water loss (diarrhea). Citrinin infusion caused increased urine flow rate, increased urine flow rate/GFR, increased FWC, increased Na excretion, and decreased urine osmolality. Pretreatment with OA attenuated these effects of citrinin, presumably due to renal compensation for the OA-induced hemoconcentration. Citrinin and OA do not appear to have additive diuretic effects during the first 48 h of toxin exposure.

Animals↗
PubMedDate not supplied

Effects of citrinin on renal tubular transport functions in the rat.

The fungal toxin, citrinin, has been implicated as a nephrotoxin. Both in vitro and in vivo studies were undertaken to examine, in a controlled laboratory setting, the effects of citrinin on overall renal function as well as on specific renal transport processes. At a dose of 70 mg/kg citrinin caused an increase in urine production and a decrease in urine osmolality in the Sprague-Dawley rat. Maximal effects were observed at 4 days after a single dose, and animals surviving for that time period regained normal renal function by 5--8 days. Animals that failed to survive first entered a period of oliguria or anuria. Fischer 344 rats did not demonstrate an unusual sensitivity to citrinin. Renal slice transport of various organic compounds, e.g., paminohippurate (PAH) and tetraethylammonium (TEA), also was inhibited with maximal effects seen at day 4. In vitro effects of citrinin on fresh renal tissue were different, in part, from the effects seen with pretreatment. No alterations of renal cortical inorganic electrolytes were observed.

Animals↗
PubMedDate not supplied

Mechanism of citrinin-induced dysfunction of mitochondria. III. Effects on renal cortical and liver mitochondrial swelling.

The effects of the mycotoxin citrinin on renal cortical and liver mitochondrial swelling were studied. Citrinin decreases the rate of swelling induced by the valinomycin-K+ complex, suggesting that the mycotoxin interferes with the mitochondrial membrane fluidity. Citrinin promotes reduction of the amplitude of swelling in the presence of Na+ ions. This alteration reflects interference with complex I of the respiratory chain and ATP synthase complex activity without disarranging the inner mitochondrial membrane, in view of the fact that the shrinkage was not affected. The effect increases with citrinin concentration. Renal tissue is more susceptible than hepatic tissue.

Animals↗
PubMed1984

Renal and hepatic glutathione concentrations in rats after treatment with hexachloro-1,3-butadiene and citrinin.

Renal and hepatic glutathione (GSH) concentrations were examined after treatment of male Sprague-Dawley rats with hexachloro-1,3-butadiene (HCBD) or citrinin alone and in combination, and after pretreatment with the GSH depleting agent diethylmaleate (DEM). It was found that both renal and hepatic GSH depletion were greater when either citrinin or HCBD was given following DEM. The effect was particularly striking when the doses used were so low as to be ineffective when given alone. When HCBD and citrinin were given in combination, the effect on GSH was approximately additive. Renal tubular organic ion transport in kidney slices was also compromised significantly when either citrinin or HCBD followed pretreatment with DEM. With HCBD, depression of tetraethylammonium (TEA) transport was seen after DEM; when given alone HCBD had no effect on TEA transport.

Animals↗
PubMed1976

Antiprotozoal activity in citrinin.

Citrinin has an inhibitory effect on growth of T. pyriformis. Citrinin also caused a shift to smaller cell size, particularly at the higher concentrations (25, 50 and 100 mug/ml). The mycotoxin exerted only a marginal effect on the respiration of T. pyriformis; but citrinin (25 mug/ml) induced an inhibitory effect on DNA, RNA and protein content. The greatest decrease was in RNA, while smaller decreases in protein and DNA were observed. A bioassay employing T. pyriformis was determined; the lower limit of citrinin detection was between 1 and 5 mug/ml.

Animals↗
PubMed1993

Influences of chemical fertilizers (in vitro) on aflatoxin and citrinin synthesis by two strains of aspergilli.

The selective effect of various levels of phosphate and nitrate (as fertilizers) on biosynthesis of aflatoxin by Aspergillus parasiticus var. globosus, and citrinin by A. terreus var. aureus was studied in defined culture medium. Phosphate at 35-175 mmol per 50 mL decreased aflatoxin production, but increased citrinin synthesis. Nitrate at 73-365 mmol per 50 mL stimulated the synthesis of aflatoxin but depressed that of citrinin. A rise in the levels of nitrate and phosphate led to a decrease in aflatoxin production, an increase in citrinin production and an accumulation of mycelial phosphate and nitrate contents.

Aflatoxins↗
PubMed1996

Simple and sensitive high-performance liquid chromatography--fluorescence method for the determination of citrinin application to the analysis of fungal cultures and cheese extracts.

A new and highly sensitive method for the detection of the important mycotoxin, citrinin, has been developed. Spectroscopic studies demonstrate that the fluorescence of this metabolite is influenced by the pH of the environment. This fact was exploited in the chromatographic determination of citrinin with fluorescence detection. The proposed method, based on the addition of 1 M hydrochloric acid as an acidic post-column reagent, has a limit of detection of 0.9 center dot 10(-7) M. Analytical validation shows that linearity can be assumed from 2 center dot 10(-7) to 10(-4) M citrinin. The repeatability and reproducibility are satisfactory, with R.S.D. = 5.1% (n = 9, c = 10(-5) M) and R.S.D. = 7.2% (n = 9, c = 10(-5) M). The method was also applied to the determination of this mycotoxin produced by mould cultures isolated from soft cheese and also from soft cheese and also from cheese extracts spiked with citrinin. The specificity of the method is demonstrated and the necessity for post-column acidification is illustrated on real samples.

Cheese↗