Ochratoxin B

369.37

369.37

200-835-2

ECJ5WS94N2

3462

DTXSID1075301

Crystals from methanol|Exhibits blue fluorescence

39229000

112.93000

3.06

Crystals that exhibit blue fluorescence. (NTP, 1992)

1.4±0.1 g/cm3

221 °C

632.4±55.0 °C at 760 mmHg

-11 °C

1.623

In water, 4.40 mg/L at 25 deg C (est)

2-8°C

6.39X10-15 mm Hg at 25 deg C (est)

Oral-chicken LD50: 54 mg/kg

Flammable, decomposes toxic nitrogen oxides and chloride gases when burned

D -35° (c = 0.15 in ethanol)

pKa1 = 3.3 (carboxyl); pKa2 = 7.0 (hydroxyl) (est)

No rapid reaction with air. No rapid reaction with water.

Acids, Carboxylic

OCHRATOXIN B is incompatible with strong oxidizing agents, strong acids and strong bases. It is a carboxylic acid derivative. Carboxylic acids donate hydrogen ions if a base is present to accept them. They react in this way with all bases, both organic (for example, the amines) and inorganic. Their reactions with bases, called "neutralizations", are accompanied by the evolution of substantial amounts of heat. Neutralization between an acid and a base produces water plus a salt.

I

6.1(a)

UN 3462 6.1/PG 3

3

22-36/37/38-65-48/23/24/25-36/38-11-46-45-36-20/21/22

26-36-45-16-53-36/37-62

AY6825000

Xn,T,F

Treasury is low temperature, ventilated, dry; stored separately from food raw materials

P210-P280-P305 + P351 + P338

H225-H302-H312-H319-H332

SRP: Criteria for land treatment or burial (sanitary landfill) disposal practices are subject to significant revision. Prior to implementing land disposal of waste residue (including waste sludge), consult with environmental regulatory agencies for guidance on acceptable disposal practices.

WHO; Environmental Health Criteria 105: Selected Mycotoxins: Ochratoxins, Trichothecenes, Ergot (1990)

Flash point data for this compound are not available. It is probably combustible. (NTP, 1992)

|Danger|H301 (100%): Toxic if swallowed [Danger Acute toxicity, oral]|P261, P264, P270, P271, P280, P301+P310, P302+P352, P304+P340, P305+P351+P338, P312, P321, P330, P332+P313, P337+P313, P362, P403+P233, P405, and P501|Aggregated GHS information provided by 39 companies from 1 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Fires involving this compound can be controlled with a dry chemical, carbon dioxide or Halon extinguisher. (NTP, 1992)

Excerpt from ERG Guide 153 [Substances - Toxic and/or Corrosive (Combustible)]: As an immediate precautionary measure, isolate spill or leak area in all directions for at least 50 meters (150 feet) for liquids and at least 25 meters (75 feet) for solids. SPILL: Increase, in the downwind direction, as necessary, the isolation distance shown above. FIRE: If tank, rail car or tank truck is involved in a fire, ISOLATE for 800 meters (1/2 mile) in all directions; also, consider initial evacuation for 800 meters (1/2 mile) in all directions. (ERG, 2016)

SMALL SPILLS AND LEAKAGE: If you spill this chemical, FIRST REMOVE ALL SOURCES OF IGNITION. You should then dampen the solid spill material with 60-70% ethanol, then transfer the dampened material to a suitable container. Use absorbent paper dampened with ethanol to pick up any remaining material. Your contaminated clothing and absorbent paper should be sealed in a vapor-tight plastic bag for eventual disposal. Solvent-wash contaminated surfaces with 60-70% ethanol followed by washing with a soap and water solution. Do not reenter the contaminated area until the Safety Officer (or other responsible person) has verified that the area has been properly cleaned. STORAGE PRECAUTIONS: You should keep this material in a tightly closed container under an inert atmosphere, and store it at refrigerated temperatures. (NTP, 1992)

RECOMMENDED RESPIRATOR: Where the neat test chemical is weighed and diluted, wear a NIOSH-approved half face respirator equipped with a combination filter cartridge, i.e. organic vapor/acid gas/HEPA (specific for organic vapors, HCl, acid gas, SO2 and a high efficiency particulate filter). (NTP, 1992)

highly toxic

/AQUATIC SPECIES/ Ochratoxin B caused no deaths in Mt. Shasta strain of rainbow trout at dose of 66.7 mg/kg bw ip. Histophathological damage of liver and kidney occurred.

Ochratoxins are toxic metabolites from Aspergillus ochraceus, A. sulphureus, A. melleus and Penicillium viridicatum. As these molds occur widely, some toxins have been found as natural contaminants on corn, peanuts, storage grains, cottonseed, and other decaying vegetation. /Ochratoxins/

Ochratoxin B's limited production and use experimentally as a teratogen and carcinogen(1) may result in its release to the environment through various waste streams(SRC).

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 300(SRC), determined from an estimated log Kow of 3.77(2) and a regression-derived equation(2), indicates that the neutral species of ochratoxin B is expected to have moderate mobility in soil(SRC). The estimated pKa values of ochratoxin B are 3.3 and 7.0(3), indicating that this compound will exist almost entirely in the anion form in the environment and anions generally do not adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(4). Volatilization from moist soil is not expected because the compound exists as an anion and anions do not volatilize. Ochratoxin B is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 6.4X10-15 mm Hg at 25 °C(SRC), determined from a fragment constant method(2). Biodegradation data in soil were not available(SRC, 2013).|AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 300(SRC), determined from an estimated log Kow of 3.77(2) and a regression-derived equation(2), indicates that the neutral species of ochratoxin B is expected to adsorb to suspended solids and sediment(SRC). Estimated pKa values of 3.3 and 7.0(3) indicate ochratoxin B will exist almost entirely in the anion form at pH values of 5 to 9 and, therefore, volatilization from water surfaces is not expected to be an important fate process(SRC). According to a classification scheme(4), an estimated BCF of 3(SRC), from its estimated log Kow(2) and a regression-derived equation(2), suggests the potential for bioconcentration in aquatic organisms is low(SRC). Ochratoxin B may undergo hydrolysis as it contains a cyclic ester functionality which can hydrolyze under environmental conditions (pH 5 to 9)(5). Biodegradation data in water were not available(SRC, 2013).|ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), ochratoxin B, which has an estimated vapor pressure of 6.4X10-15 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), is expected to exist solely in the particulate phase in the ambient atmosphere. Particulate-phase ochratoxin B may be removed from the air by wet and dry deposition(SRC). Ochratoxin B absorbs UV light at wavelengths >290 nm(3) and, therefore, may be susceptible to direct photolysis by sunlight(SRC).

Ochratoxin B may undergo hydrolysis in the environment as it contains a cyclic ester functionality which can hydrolyze under environmental conditions (pH 5 to 9)(1). Ochratoxin B absorbs UV light at wavelengths >290 nm(3) and, therefore, may be susceptible to direct photolysis by sunlight(SRC).|It has previously been shown that the biosynthesis of the mycotoxins ochratoxin A and B and of citrinin by Penicillium is regulated by light. However, not only the biosynthesis of these mycotoxins, but also the molecules themselves are strongly affected by light of certain wavelengths. The white light and blue light of 470 and 455 nm are especially able to degrade ochratoxin A, ochratoxin B and citrinin after exposure for a certain time. After the same treatment of the secondary metabolites with red (627 nm), yellow (590 nm) or green (530 nm) light or in the dark, almost no degradation occurred during that time indicating the blue light as the responsible part of the spectrum. The two derivatives of ochratoxin (A and B) are degraded to certain definitive degradation products which were characterized by HPLC-FLD-FTMS. The degradation products of ochratoxin A and B did no longer contain phenylalanine. ... The biological consequences of the light instability of the toxins are discussed.

An estimated BCF of 3 was calculated in fish for ochratoxin B(SRC), using an estimated log Kow of 3.77(1) and a regression-derived equation(1). According to a classification scheme(2), this BCF suggests the potential for bioconcentration in aquatic organisms is low(SRC).

Using a structure estimation method based on molecular connectivity indices(1), the Koc of ochratoxin B can be estimated to be 300(SRC). According to a classification scheme(2), this estimated Koc value suggests that ochratoxin B is expected to have moderate mobility in soil. The estimated pKa values of ochratoxin B are 3.3 and 7.0(3), indicating that this compound will exist almost entirely in the anion form in the environment and anions generally do not adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(4).

The estimated pKa values of 3.3 and 7.0(1) indicate ochratoxin B will exist almost entirely in the anion form at pH values of 5 to 9 and, therefore, volatilization from water surfaces is not expected to be an important fate process. Ochratoxin B is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 6.4X10-15 mm Hg(SRC), determined from a fragment constant method(2).

The presence of 34 mycotoxins in dietary supplements containing green coffee bean (GCB) extracts was determined. Ochratoxin B was found in 32% of tested products. The concentration of ochratoxin B ranged from <1.0-20.2 ug/kg(1).|Five independent episodes of ochratoxicosis in about 970,000 turkeys, two episodes in about 70,000 laying hens, and two episodes in about 12,000,000 broiler chickens were investigated. Ochratoxin A concentrations in suspect feed and ingredients ranged from <0.2 to 16 ppm. Feed samples tested for T-2 toxin, F-2 toxin, heavy metals, and polychlorinated biphenyls were negative. Minor amounts of aflatoxin (<60 ppb) were found in suspect feed from two episodes. ... Eight of the 9 episodes were traced to the corn supply and the ninth episode was traced to corn gluten meal that became contaminated during storage after manufacture. Evidence was obtained that the ochratoxin was unstable and declined in concentration during storage. ... The ochratoxin extracted from high potency samples consisted of ochratoxins A, B, and C in ratios of about 90:8:2(1).|The effects of temperature and length of incubation on ochratoxin A production in various substrates were studied. The optimal temperature for toxin production by Aspergillus ochraceus NRRL-3174 was found to be around 28 C. Very low levels of ochratoxin A are produced in corn, rice, and wheat bran at 4 C. The optimal time for ochratoxin A production depends on the substrate, ranging from 7 to 14 days at 28 C. Ochratoxin B and dihydroisocoumaric acid, i.e., one of the hydrolysis products of ochratoxin A, were produced in rice but at levels considerably lower than ochratoxin A. No ochratoxin C was produced in rice at 28 C. When added to rice cereal or oatmeal, the toxin was found to be very stable over prolonged storage and even to autoclaving for 3 hr.

Occupational exposure to ochratoxin B may occur potentially through inhalation of dusts and dermal contact at workplaces where handling of commodities such as coffee beans occurs. Monitoring data indicate that the general population is exposed to ochratoxin B predominately via ingestion of and dermal contact with food products contaminated with this compound. (SRC)

Methods for preparation of labelled ochratoxin A and B are described. The method for preparation of labelled ochratoxin B involves the synthesis of the azide of ochratoxin beta via the mixed anhydride and subsequent conjugation to labelled phenylalanine to yield (14)C-ochratoxin B. The labelled ochratoxins were injected into male Wistar rats and after different survival times they were sacrificed and subjected to whole body autoradiography. The distribution pattern of ochratoxin A in the rat did not differ from that earlier registered for mouse. The previously known, high susceptibility of rats (and not mice) to ochratoxin A-induced cancer could thus not be explained by an accumulation of the toxin in specific cells or organs. The distribution patterns of ochratoxin A and B were almost congruent--the only apparent difference being a much longer retention of the labelled ochratoxin A in the blood compared to ochratoxin B, which was much faster excreted. When analyzing tissue extracts for labelled metabolites only the extracts from the rats injected with ochratoxin B were found to contain easily detectable concentrations, while no metabolites of ochratoxin A were seen.|Mixture of ochratoxins A and B (0.38 and 0.13 mg/kg body wt) was fed to pigs daily for 8 days during early pregnancy. Ochratoxin B was poorly absorbed and preferentially hydrolyzed in intestinal tract.|... Since little is known regarding biotransformation ... of OTB, the aim of this study was to investigate biotransformation of OTB in rats... Male F344 rats were administered either a single dose of OTB (10 mg/kg bw) or repeated doses (2 mg/kg bw, 5 days/week for 2 weeks) and euthanized 72 hr after the last dosing. ... Excretion of OTB and metabolites in urine and feces was analyzed using both HPLC with fluorescence detection and LC-MS/MS. Ochratoxin beta, which results from cleavage of the peptide bond, was the major metabolite excreted in urine in addition to small amounts of 4-hydroxy-OTB. In total, 19% of the administered dose was recovered as OTB and ochratoxin beta in urine and feces within 72 hr after a single dose. In contrast to OTA, no tissue-specific retention of OTB was evident after single and repeated administration. ... OTB is more extensively metabolized and more rapidly eliminated than OTA. ...

... Since little is known regarding biotransformation ... of OTB, the aim of this study was to investigate biotransformation of OTB in rats... Male F344 rats were administered either a single dose of OTB (10 mg/kg bw) or repeated doses (2 mg/kg bw, 5 days/week for 2 weeks) and euthanized 72 hr after the last dosing. ... Excretion of OTB and metabolites in urine and feces was analyzed using both HPLC with fluorescence detection and LC-MS/MS. Ochratoxin beta, which results from cleavage of the peptide bond, was the major metabolite excreted in urine in addition to small amounts of 4-hydroxy-OTB. In total, 19% of the administered dose was recovered as OTB and ochratoxin beta in urine and feces within 72 hr after a single dose. In contrast to OTA, no tissue-specific retention of OTB was evident after single and repeated administration. ... OTB is more extensively metabolized and more rapidly eliminated than OTA. ...|Ochratoxin B (0.13 mg/kg body wt) fed to pigs daily for 8 days was completely hydrolyzed to ochratoxin beta.|A metabolic product was formed from ochratoxin B by rat liver microsomal fractions in the presence of NADPH. It was isolated from the incubation mixture by extraction, thin-layer chromatography, high-pressure liquid chromatography, and crystallization. On the basis of mass and nuclear magnetic resonance spectroscopy, the structure is suggested to be 4-hydroxyochratoxin B. The Km for the formation of 4-hydroxyochratoxin B was determined, and the hydroxylation of ochratoxin A was not altered by the presence of ochratoxin B. Rats were given ochratoxin A or B, or a mixture of both intraperitoneally. The ratios of the three metabolites, ochratoxin A, (4R)-4-hydroxyochratoxin A, and ochratoxin alpha, excreted in the urine did not change in the presence of ochratoxin B. Ochratoxin B was metabolized to 4-hydroxyochratoxin B and ochratoxin beta, but in a different ratio than for the ochratoxin A metabolites. When given intraperitoneally, ochratoxin beta was excreted within 24 hr. In rats treated with ochratoxin A alone, the food intake was reduced by 50%, and histologically severe lesions, degeneration, and necrosis were observed in the proximal tubules. When ochratoxin A and B given in combination, the animals were clinically unaffected and histologically there was only slight damage of proximal tubules. These observations indicate that ochratoxin B considerably reduces the toxic effects of ochratoxin A.|The objectives of this study were to develop and evaluate procedures for the confirmation of ochratoxin A (OA), lactone opened OA (OP-OA), ochratoxin B (OB), hydroxy OA (OA-OH) and ochratoxin alpha (Oalpha) and metabolites formed in the rats from these toxins, and to demonstrate that many ochratoxin metabolites can be identified in the bile and urine of rats injected with the different ochratoxins. An esterification procedure in acidified methanol and a lactone hydrolysis procedure in strong base yielded two additional forms of most of the different ochratoxins. The esterification procedure provided a simple, fast and reliable method for the confirmation of the ochratoxins. A total of 20 different metabolites of OA, OP-OA, OB, OA-OH and Oalpha were detected in the urine and the bile of rats of which several were identified. Among these, OA and the recently discovered and toxic form of OA (OP-OA) were readily formed in vivo when either were injected. Procedures developed in this study can be used to confirm and isolate ochratoxins in biological samples and have shown that a new form of OA (OP-OA) along with many other metabolites are formed from OA and related ochratoxins in vivo.

Excerpt from ERG Guide 153 [Substances - Toxic and/or Corrosive (Combustible)]: TOXIC; inhalation, ingestion or skin contact with material may cause severe injury or death. Contact with molten substance may cause severe burns to skin and eyes. Avoid any skin contact. Effects of contact or inhalation may be delayed. Fire may produce irritating, corrosive and/or toxic gases. Runoff from fire control or dilution water may be corrosive and/or toxic and cause pollution. (ERG, 2016)

EYES: First check the victim for contact lenses and remove if present. Flush victim's eyes with water or normal saline solution for 20 to 30 minutes while simultaneously calling a hospital or poison control center. Do not put any ointments, oils, or medication in the victim's eyes without specific instructions from a physician. IMMEDIATELY transport the victim after flushing eyes to a hospital even if no symptoms (such as redness or irritation) develop. SKIN: IMMEDIATELY flood affected skin with water while removing and isolating all contaminated clothing. Gently wash all affected skin areas thoroughly with soap and water. If symptoms such as redness or irritation develop, IMMEDIATELY call a physician and be prepared to transport the victim to a hospital for treatment. INHALATION: IMMEDIATELY leave the contaminated area; take deep breaths of fresh air. IMMEDIATELY call a physician and be prepared to transport the victim to a hospital even if no symptoms (such as wheezing, coughing, shortness of breath, or burning in the mouth, throat, or chest) develop. Provide proper respiratory protection to rescuers entering an unknown atmosphere. Whenever possible, Self-Contained Breathing Apparatus (SCBA) should be used; if not available, use a level of protection greater than or equal to that advised under Protective Clothing. INGESTION: If the victim is conscious and not convulsing, give 1 or 2 glasses of water to dilute the chemical and IMMEDIATELY call a hospital or poison control center. Generally, the induction of vomiting is NOT recommended outside of a physician's care due to the risk of aspirating the chemical into the victim's lungs. However, if the victim is conscious and not convulsing and if medical help is not readily available, consider the risk of inducing vomiting because of the high toxicity of the chemical ingested. Ipecac syrup or salt water may be used in such an emergency. IMMEDIATELY transport the victim to a hospital. If the victim is convulsing or unconscious, do not give anything by mouth, ensure that the victim's airway is open and lay the victim on his/her side with the head lower than the body. DO NOT INDUCE VOMITING. IMMEDIATELY transport the victim to a hospital. OTHER: Since this chemical is a known or suspected carcinogen you should contact a physician for advice regarding the possible long term health effects and potential recommendation for medical monitoring. Recommendations from the physician will depend upon the specific compound, its chemical, physical and toxicity properties, the exposure level, length of exposure, and the route of exposure. (NTP, 1992)

/SRP:/ Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR if necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on the left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Poisons A and B/|/SRP:/ Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if needed. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool ... . Cover skin burns with dry sterile dressings after decontamination ... . /Poisons A and B/|/SRP:/ Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Positive-pressure ventilation techniques with a bag valve mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Treat seizures with diazepam or lorazepam ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poisons A and B/

/GENOTOXICITY/ To elucidate the effects of three structurally related mycotoxins, namely, ochratoxin A (OTA), ochratoxin B (OTB), and citrinin (CIT), on human health, ...their acute toxic, mitogenic, and genotoxic effects in the human-derived liver cell line (HepG2) /were investigated/. These compounds are found in moldy foods in endemic areas of nephropathy, which is associated with urinary tract cancers. In agreement with previous experiments, /investigators/ found that OTA causes a dose-dependent induction of micronuclei (MN) and DNA migration in the single-cell gel electrophoresis (SCGE) assay, which was statistically significant at concentrations of > or =5 ug/mL. In contrast, OTB was devoid of genotoxic activity under identical conditions, but the compound caused pronounced inhibition of cell division even at doses lower than OTA (10 ug/mL). CIT caused an effect similar to that of OTA in MN assays (significant at dose levels of > or =2.5 ug/mL) but was negative in the SCGE test. All compounds failed to induce mutations in Salmonella/microsome assays in strains TA98 and TA100 after addition of HepG2-derived enzyme homogenate (S9-mix). By use of DNA-centromeric probes /investigators/ found that induction of MN by OTA involves chromosome breaking effects (55-60% of the MN were centromere negative), whereas CIT-induced MN were predominantly centromere positive (78-82%). /These/ findings indicate that OTB is devoid of genotoxic activity in human-derived cells and therefore probably not a genotoxic carcinogen in humans. In contrast, CIT was an equally potent inducer of MN in HepG2 cells as OTA, but this effect is caused by a different mechanism, namely, aneuploidy.

ochratoxin B

Dichlorvos at 1 mg/100 mL of yeast extract-sucrose medium decreased production of ochratoxin b in cultures of Aspergillus ochraceus by 50%, but growth of culture was not affected. Concentrations of 10-30 mg/100 mL, dichlorvos decreased production of ochratoxin b 50-90%; growth was decreased 9-21%.|Isolations: van Walbeek et al, Can J Microbiol 14, 131 (1968); Shotwell et al, Appl Microbiol 17, 765 (1969); Nesheim, J Assoc Offic Anal Chem 52, 975 (1969); Natori et al, Chem Pharm Bull 18, 2259 (1970). /Ochratoxins/|As these molds occur widely, some toxins have been found as natural contaminants on corn, peanuts, storage grains, cottonseed, and other decaying vegetation. /Ochratoxins/|Ochratoxion B ... /is/ the less toxic ... /non-chlorinated/ derivative of ochratoxin A.|Two strains of Aspergillus ochraceus isolated from country cured hams produced ochratoxin B on rice, defatted peanut meal, and country cured ham.

The paper reported a reliable analytical method for simultaneous determination of ochratoxin A (OTA) and ochratoxin B (OTB) in traditional Chinese medicines (TCMs) by ultra-high-performance liquid chromatography-tandem mass spectrometry (UHPLC-MS/MS). The development of the method and investigations on the matrix influence were described in particular. The matrix effects were thereby minimized by using a reliable internal standard and a simple sample pretreatment. The established method was further validated by determining the linearity (R(2) > or = 0.9990), average recovery (86.3-114.2%), sensitivity (limit of quantitation 0.03-0.19 ng mL(-1)) and precision (relative standard deviation < or = 13.1%). It was shown to be a suitable method for simultaneous determination of OTA and OTB in various TCMs. Finally, a total of 51 TCMs widely used in China were screened for OTA and OTB with the proposed method. The results showed that only 4 samples were contaminated with ochratoxins at low levels, indicating that it was low risk of ochratoxins to consumers who occasionally used TCMs.|Methods using high-performance liquid chromatography with fluorescence detection (HPLC-FL) and using liquid chromatography with tandem mass spectrometry (LC/MS/MS) were developed for simultaneous determination of ochratoxin A (OTA), ochratoxin B (OTB) and citrinin (CIT) in cereal, fruit, and coffee products. The samples were extracted with ethyl acetate under an acidic condition, and then cleaned up with liquid-liquid separation. The test solutions were analyzed by reverse-phase HPLC-FL and LC/MS/MS. Mass spectral acquisition was performed in positive ion mode by applying multiple reaction monitoring. The performances of both detectors were almost equivalent. The recoveries of OTA and OTB were 87-111%, and that of CIT were 70-88%. The limits of quantification (S/N> or =10) of OTA, OTB and CIT was 0.1 ug/kg or less. These methods were considered to be useful for the determination of the three mycotoxins at low levels (0.1 ug/kg).|In barley & green coffee by thin layer chromatography.|Analysis of ochratoxin b in barley, using partition and thin layer chromatography.|For more Analytic Laboratory Methods (Complete) data for OCHRATOXIN B (6 total), please visit the HSDB record page.

Methods ... have been reported for determining ochratoxins in blood, e.g., by fluorescence with HPLC confirmation. /Ochratoxins/|This paper presents a simple method for the determination of ochratoxins A (OTA) and B (OTB) in pig blood serum. The method includes serum acidification (pH < 1.6) and precipitation of protein with 15% trichloroacetic acid, liquid partitioning with dichloromethane and fluorescence detection. The estimated detection limits were 0.1 ng OTA/mL and 0.2 ng OTB/mL. The mean recoveries from artificially contaminated samples (n = 6 replicates/mycotoxin) spiked at 0.3, 1 and 3 ng OTA and OTB/mL, respectively, were 86.8% (s.d. = 8.4) for OTA and 90.0% (s.d. = 9.8) for OTB. Forty-nine Romanian pig blood serum samples (94% of 52 analyzed) were found to be naturally contaminated with OTA in the range 0.1-13.4 ng/mL. No sample was found positive for OTB. The method is technically simple, specific, cost effective, suitable for large sample throughput and requires small amount of sample and reagents. It fulfills the criteria for a routine method and could be a suitable tool for surveying OTA in pig herds and in slaughtered pigs.