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At least 19 recordsLinked to original sources
PubMed1979

Determination of mycophenolic acid, penicillic acid, patulin, sterigmatocystin, and aflatoxins in cheese.

A method has been developed for detection of aflatoxins, mycophenolic acid, patulin, penicillic acid, and sterigmatocystin in cheese. It is based on selective extraction with a mixture of equal volumes of 5% sodium chloride, methanol, and aceton, precipitation of caseins at -25 C, defatting with hexane, and removal of extraneous matter by transfer of mycotoxins to chloroform and ethyl acetate. The extract is purified further by column chromatography. Mycotoxins are quantitated on thin layer chromatograms by fluorescence comparisons. Mycophenolic acid, patulin, and penicillic acid are visualized with diethylamine. The limits of detection in cheese are about 20 micrograms/kg for mycophenolic acid, patulin, and sterigmatocystin, 30 microgram/kg for pencillic acid, and 1 microgram/kg for aflatoxins B1 and M1.

Aflatoxins↗
PubMed1997

Formation and disappearance of mycophenolic acid, patulin, penicillic acid and PR toxin in maize silage inoculated with Penicillium roqueforti.

Maize silage was inoculated with Penicillium roqueforti strains which are able to form the mycotoxins mycophenolic acid (MPA), patulin (PAT), penicillic acid (PA), or PR toxin (PRT). The silage was incubated for 160 d without agitation under aerobic conditions at 15 degrees C in the dark. The mycotoxins were quantified by HPLC and identified by HPLC combined with diode array detection and by two-dimensional thin layer chromatography. MPA, PAT, PA, and PRT above the detection limit were measured for the first time at 36, 22-27, 13, and 49 days of incubation, maximum toxin contents (mg/kg) were 3.56 MPA, 15.10 PAT, 3.06 PA, and 2.17 PRT. With increasing storage time toxin contents decreased to a low or non detectable level. The production of MPA, PAT and PRT was preceded by an increase in pH from 4 to 8-9. Along with the initial pH increase the content of ergosterol as well as of P. roqueforti and yeast propagules increased whereas the levels of total soluble sugar and of water extractable NH3 decreased. It is concluded that the probability to detect MPA, PAT, PA, and PRT in maize silage moulded by P. roqueforti under practical conditions of agriculture is low during the growth of this fungus and again after prolonged storage.

Animals↗
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↗
PubMed1982

Inhibition of pancreatic carboxypeptidase A: A possible mechanism of interaction between penicillic acid and ochratoxin A.

Penicillic acid and ochratoxin A are environmentally important toxic fungal metabolites (mycotoxins) that are synergistic in combination. The effects of penicillic acid on the pancreatic enzyme, carboxypeptidase A were investigated in vitro and in vivo. A broad range of inhibition in vitro of the enzyme by PA was demonstrated with a half-maximal inhibitory concentration equal to 1.1 x 10(-4) M PA. Inhibition of carboxypeptidase A was time and temperature dependent, and resulted in decreased conversion of parent ochratoxin A to the non-toxic metabolite, ochratoxin alpha. Studies in vivo demonstrated a penicillic acid-dependent inhibition of pancreatic carboxypeptidase A activity in the mouse and the chicken following multiple oral exposure. It is postulated that the mode of toxic interaction of the two mycotoxins may be due, in part, to impaired detoxification of ochratoxin A through penicillic acid depletion of carboxypeptidase A activity.

Animals↗
PubMed2004

New antifungal activity of penicillic acid against Phytophthora species.

Penicillic acid was isolated from a culture filtrate of Aspergillus sclerotiorum. It had a high in vitro antifungal activity against Phytophthora spp., which has not been previously reported. MICs of penicillic acid were from 1 to 25 microg ml(-1) against Phytophthora spp. Penicillic acid induced abnormal branch formation, apical branching, and swelling in P. capsici, in P. cactorum mycelia contained irregular branching and small spherical swelling at apices, in P. cambivora there was irregular branching and swelling, and in P. drechsleri there was irregular multiple spherical swelling at or near hyphal apices.

Antifungal Agents↗
PubMed1986

Toxicity of penicillic acid for rat alveolar macrophages in vitro.

Penicillic acid (PA) is a polyketide mycotoxin produced by several species of Aspergillus and Penicillium. This mycotoxin is toxic in experimental animals and has also been reported to be carcinogenic. The cytotoxicity of penicillic acid was studied in rat alveolar macrophages (AM) in vitro. The effects of penicillic acid on membrane integrity were studied by measuring cell volume changes and 51Cr release. There was significant 51Cr release after 2 hr exposure to 1.0 mM penicillic acid, but not after 1 hr exposure. There was a significant decrease in adenosine triphosphate (ATP) in cell cultures exposed to 1.0 mM penicillic acid for 4 hr. Inhibition of the incorporation of [3H]leucine into protein was both dose- and time-dependent and protein synthesis was inhibited significantly after 2 hr exposure to greater than or equal to 0.1 mM penicillic acid. RNA synthesis was inhibited to a lesser extent than protein synthesis. Although there was a significant inhibition of RNA synthesis at 1.0 mM PA after 4 hr, there was no inhibition of RNA synthesis even after 4 hr at any concentration less than 1.0 mM. The ED50 dose after 2 hr exposure was 0.18 and 0.60 mM for protein and RNA synthesis, respectively. There was significant inhibition of phagocytosis after 2 hr exposure at greater than or equal to 0.3 mM penicillic acid and the ED50 for phagocytosis was 0.09 mM. Thus phagocytosis was more sensitive to the toxic effects of penicillic acid than any other cellular process studied. The results reported in this study are similar to those observed for patulin in an earlier study from our laboratory except that patulin was generally more toxic to alveolar macrophages than penicillic acid. The data demonstrate that penicillic acid is toxic to rat alveolar macrophages in vitro and suggest the possibility of a respiratory hazard to agricultural workers exposed to contaminated grain.

Adenosine Triphosphate↗
PubMed1977

Acute toxicity of penicillic acid and rubratoxin B in dogs.

The effect of intraperitoneally administered penicillic acid, a mycotoxin produced by several species of Penicillium and Aspergillus, on female dogs of mixed breeding was determined by serum tests, by observation of clinical signs and survival times, and by evaluation of gross and microscopic lesions. Combination studies employing penicillic acid and a second mycotoxin, rubratoxin B, also were undertaken. Post mortem examination disclosed hemorrhaging of the serosal surfaces of the abdomen of dogs receiving penicillic acid. The most significant histologic change observed in penicillic-acid-treated dogs was congestion and dilatation of hepatic sinusoids. Extensive hepatic changes of the liver were noted only in the dog receiving 20 mg/kg penicillic acid. There was no evidence of parenchymal necrosis in any of the liver samples examined from animals given penicillic acid. A predominently peripheral lobular depletion of glycogen in parenchymal cytoplasm also was seen in liver sections from animals exposed to penicillic acid. Although slight decreases in lactic dehydrogenase were observed, no trends were detected in the several blood enzymes and serum constituents examined that could be specifically related to penicillic acid intoxification. Glutamic-oxaloacetic transaminase, lactic dehydrogenase and alkaline phosphatase activities and survival time varied in relation to duration of exposure and total dose of rubratoxin B administered. The lesions in animals injected with 1.0 mg/kg rubratoxin B consisted of mild hepatic necrosis and degenerative changes in renal tubular epithelium. An additive effect due to the combined administration of penicillic acid and rubratoxin B was observed only by an elevation in serum sodium and chlorine levels.

Alkaline Phosphatase↗
PubMed2006

Production of penicillic acid by Aspergillus sclerotiorum CGF.

The production of penicillic acid by Aspergillus sclerotiorum CGF for the biocontrol of Phytophthora disease was investigated in submerged fermentation using media composed of different nutrients. Soluble starch was found to be the most effective substrate among the carbon sources used, and produced the highest penicillic acid concentration of 2.98 mg ml(-1). When organic nitrogen sources were used, pharmamedia, yeast extract, and polypeptone-S were found to be suitable organic nitrogen sources (2.46-2.71 mg ml(-1)). The production of penicillic acid was not detected in when inorganic nitrogen sources were used. Only Na2HPO4, among the metal ions and phosphate salts tested, increased the production of penicillic acid (approximately 20%). When A. sclerotiorum CGF was cultured in optimal medium [8.0% (w/v) soluble starch, 0.6% (w/v) yeast extract, and 0.3% (w/v) Na2HPO4], maximum penicillic acid concentration (approximately 9.40 mg ml(-1)) and cell mass (approximately 17.4 g l(-1)) were obtained after 12 days.

Aspergillus↗
PubMed1980

Evaluation of penicillic acid for toxicity in broiler chickens.

Penicillic acid is a mycotoxin produced by various fungi. It may occur in high concentrations in corn and can also be produced concomitantly with other mycotoxins in poultry feed. This mycotoxin was evaluated for its toxicity in broiler chickens by feeding graded concentrations (0, 100, 200, and 400 microgram/g of diet) to 4 groups of 10 birds per treatment. No significant (P greater than .05) effects were measured on growth rate, feed conversion, relative size of pancreas, spleen, liver, heart, bursa, or kidney or on hemoglobin, packed cell volume, liver lipid, plasma protein, or glucose. The only significant effects were a slight reduction in the size of the proventriculus and gizzard at dose levels of 200 and 400 microgram/g. Neither the salt nor lactone forms of penicillic acid had any detectable effect. The acute oral LD50 for the sodium salt form was 92 +/- 9 mg/kg. These data suggest that penicillic acid by itself has little toxicity (less than 1% of that of aflatoxin) in chickens.

Animals↗
PubMed1987

6-Methyl-1,2,4-benzenetriol, a new intermediate in penicillic acid biosynthesis in Penicillium cyclopium.

Penicillic acid-negative mutants were obtained from a color mutant derived from Penicillium cyclopium NRRL 1888 through N-methyl-N'-nitro-N-nitrosoguanidine treatment. One mutant (SK2N6) accumulated 6-methyl-1,2,4-benzenetriol, which was not previously known to be a metabolite of P. cyclopium, in addition to orsellinic acid and orcinol. The radioactivity of [1-14C]acetic acid was rapidly incorporated into 6-methyl-1,2,4-benzenetriol in a culture of P. cyclopium SK2N6. Moreover, the radioactivity of [14C]6-methyl-1,2,4-benzenetriol was efficiently incorporated into penicillic acid in a culture of P. cyclopium NRRL 1888. These data indicate that 6-methyl-1,2,4-benzenetriol is a precursor for penicillic acid biosynthesis. The results on the addition of 1,4-dihydroxy-6-methoxy-2-methylbenzene, 6-methoxy-2-methylbenzoquinone(1,4), and 1-O-methylorcinol to a culture of P. cyclopium SK2N6 indicated that only the former two compounds are converted to penicillic acid. Thus, a new portion of the penicillic acid biosynthetic pathway is proposed.

Caproates↗
PubMed1987

Bacterial tests as indicators for the detoxification of the mycotoxin penicillic acid by ammonia treatment.

The detoxification of penicillic acid by reaction with ammonia was examined by means of a polymerase assay using two strains of Escherichia coli (pol A+ and pol A-1) and a recombination assay using two strains of Bacillus subtilis (rec+ and rec-). A 100-fold surplus of ammonia added to penicillic acid abolished the cytotoxic and genotoxic effects of penicillic acid towards the bacteria under the test conditions. The study presents the possibility of detoxifying mycotoxins in feeds by ammonia treatment and demonstrates the suitability of bacterial assays as indicators for mycotoxins.

Ammonia↗
PubMed1981

High pressure liquid chromatographic determination of penicillic acid in chicken tissues.

Penicillic acid (PA) is a mycotoxin with reported cytotoxic, cardiotoxic, and carcinogenic activity and it can occur in high concentration in corn. The occurrence of PA in contaminated poultry feed represents a potential public health hazard. A reverse phase high pressure liquid chromatographic (HPLC) method is proposed for determining PA residues in chicken tissues. Optimization of chromatography was achieved for PA using a mobile phase consisting of acetonitrile: H2O. PA was detected by ultraviolet absorption at 254 nm, identified by retention time, and quantitated by peak area integration. Blood, parenchymal tissues, muscle, and alimentary tract contents were homogenized, sonicated, and acid treated followed by extraction with ethyl acetate and analysis by HPLC. Acute oral dosing of chickens with PA over a range of 50 to 550 mg/kg body weight resulted in detectable levels of the mycotoxin (confirmed by gas liquid chromatography) in gizzard muscle and contents, liver, kidney, heart, and intestinal contents. This method should prove useful both for the rapid and sensitive detection of PA residues in poultry and in further studies on the distribution and metabolism of this mycotoxin.

Animals↗
PubMed1981

Ochratoxin A and penicillic acid interaction in mice.

Penicillic Acid (PA) and Ochratoxin A (OA) are toxic fungal metabolites that are synergistic in combination. This interaction was investigated using mice which were doses orally as follows: control, none; solvent control, 0.2 ml bicarbonate buffer; PA, 40 mg/kg; OA, 10 mg/kg and combination, 40 mg/kg PA + 10 mg/kg OA. The only significant histopathologic change observed was an acute multifocal toxic tubular nephrosis which appeared most severe in the combination-treated mice killed on day 10. While the combination group had a death rate of 20% (5/25), no deaths occurred in the other treatment groups. The increased death rate and the extensive nephrotoxic findings in the combination group indicate a toxic interaction between OA and PA at sublethal dose levels and is consistent with a renal site of action.

Animals↗
PubMed1978

Preliminary report of the distribution of [14C]penicillic acid in rats: autoradiographic technique.

The distribution of [14C]penicillic acid in rats was determined by autoradiographic technique. Adult male rats were given [14C]penicillic acid orally and IV. According to autoradiographic analyses 24 hours later, high levels of radioactivity were in liver, heart, kidneys, lungs, and caudal part of the intestine. The significance of bile as an excretory route for penicillic acid was confirmed by the results from IV administration of the compound.

Administration, Oral↗
PubMed1980

In vivo and in vitro metabolism of [14C]penicillic acid.

In vivo and in vitro studies of the metabolism of [14C]penicillic acid showed a significant uptake of penicillic acid by red blood cells and a significant increase in radioactivity associated with the membrane fraction with time (1-4 hr); however, the majority of the red blood cell activity was intracellular. The 14C-radioactivity concentration in liver fractions (1.5 percent of the administered dose 2 hr following administration) was high in the RNA-DNA and protein fractions. The level of the 14C activity associated with these fractions increased with time (24 hr). Preliminary studies of the in vivo metabolism of [14C]penicillic acid by rats showed that a significant amount of radioactivity was excreted in the urine (82 percent of the administered dose after 7 days), of which strongly acidic urinary metabolites accounted for 23 percent; weakly to moderately acidic, 60 percent; strongly basic, 2 percent; and neutral, 15 percent. Isolation and identification studies of the neutral urinary fraction indicated that the major metabolites are non-ionic macromolecules (Mr < 5000). Biliary metabolites (10 percent of the administered dose 2 hr following administration) were 28 percent strongly acidic and 72 percent weakly to moderately acidic.

Absorption↗