Aflatoxin G1

328.27

328.27

214-615-9

DTXSID4020036

Crystals ... exhibits green fluorescence

84.20000

-0.17

Solid

1.6±0.1 g/cm3

244-246 °C

612.1±55.0 °C at 760 mmHg

-11 °C

1.680

Aflatoxins ... are soluble in methanol, acetone, and chloroform, but only slightly soluble in water and hydrocarbon solvents.

2-8°C

5.86X10-11 mm Hg at 25 °C (est)

Peritoneal-rat LD50: 14.9 mg/kg; oral-duck LD50: 2.45 mg/kg

Flammable; burning releases irritating fumes

D -556° (chloroform)

Henry's Law constant = 4.96X10-13 cu cm/molec-sec at 25 °C (est)

164 Ų [M+H]+ [CCS Type: TW, Method: calibrated with polyalanine]|176.5 Ų [M+Na]+ [CCS Type: TW, Method: calibrated with polyalanine]|180.2 Ų [M+K]+ [CCS Type: TW, Method: calibrated with polyalanine]

Aflatoxins are densely fluorescent; the B refers to blue, while the G signifies green fluorescence. /Aflatoxins/

I

6.1(a)

UN 3462 6.1/PG 1

3

45-26/27/28-65-48/23/24/25-36/38-11-46-39/23/24/25-23/24/25-36-20/21/22

53-28-36/37-45-62-26-16-7-36

LV1720000

T+,T,F,Xn

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

Relatively unstable to light & air, particularly in soln in highly polar solvents; chloroform solutions are stable for years if kept in dark & cold.

P201-P210-P301 + P310-P305 + P351 + P338-P308 + P313-P331

H225-H304-H315-H319-H340-H350-H372

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.|Chemical treatment: Any chemical detoxification must reduce the mycotoxin level to within limits set by proper regulatory agencies, must have no toxic residues, and should not decrease the nutritive value of the treated commodity. These restrictions as well as simple economic considerations have narrowed the types of chemical agents likely to achieve significance in a commercially scaled detoxification process. Chemicals having good promise in this regard can be classified simply as oxidizing agents, acid, and bases. Of oxidizing systems that destroy all the aflatoxin only hydrogen peroxide has shown promise to detoxify foods and feeds. ... Aqueous suspensions of peanut meals containing 90 ppm aflatoxin /were treated/ with 6% soln of hydrogen peroxide at pH 9.5 for 30 min at 80 °C. The treatment destroyed 97% of the toxin ... . The use of acids as detoxifying agents has a definite potential in the recovery process of free fatty acids from commercial soapstock prepn. The use of inorganic and organic bases affords an efficient and relatively inexpensive means to achieve aflatoxin destruction or removal from large quantities of contaminated agricultural commodities. The refinement of edible oils is a classic example of the use of bases under conditions that would destroy or remove aflatoxins.|PRECAUTIONS FOR "CARCINOGENS": There is no universal method of disposal that has been proved satisfactory for all carcinogenic compounds & specific methods of chem destruction ... published have not been tested on all kinds of carcinogen-containing waste. ... summary of avail methods & recommendations ... /given/ must be treated as guide only. /Chemical Carcinogens/|PRECAUTIONS FOR "CARCINOGENS": ... Incineration may be only feasible method for disposal of contaminated laboratory waste from biological expt. However, not all incinerators are suitable for this purpose. The most efficient type ... is probably the gas-fired type, in which a first-stage combustion with a less than stoichiometric air:fuel ratio is followed by a second stage with excess air. Some ... are designed to accept ... aqueous & organic-solvent solutions, otherwise it is necessary ... to absorb soln onto suitable combustible material, such as sawdust. Alternatively, chem destruction may be used, esp when small quantities ... are to be destroyed in laboratory. /Chemical Carcinogens/|For more Disposal Methods (Complete) data for AFLATOXIN G1 (7 total), please visit the HSDB record page.

U.S. Department of Health & Human Services/National Toxicology Program; Twelfth Report on Carcinogens (2011). The Report on Carcinogens is an informational scientific and public health document that identifies and discusses substances (including agents, mixtures, or exposure circumstances) that may pose a carcinogenic hazard to human health. Aflatoxins (1402-68-2) are known to be human carcinogens. First listed in the First Annual Report on Carcinogens (1980). /Aflatoxins/[Available from, as of July 25, 2013: http://ntp.niehs.nih.gov/]|WHO; Environmental Health Criteria 11: Mycotoxins (1979)

|Danger|H300+H310+H330 (100%): Fatal if swallowed, in contact with skin or if inhaled [Danger Acute toxicity, oral; acute toxicity, dermal; acute toxicity, inhalation]|P201, P202, P260, P262, P264, P270, P271, P280, P281, P284, P301+P310, P302+P350, P304+P340, P308+P313, P310, P320, P321, P322, P330, P361, P363, P403+P233, P405, and P501|Aggregated GHS information provided by 4 companies from 1 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.|H300: Fatal if swallowed [Danger Acute toxicity, oral]|P201, P202, P260, P264, P270, P281, P301+P310, P307+P311, P308+P313, P314, P321, P330, P405, and P501

Skin and body protection: Complete suit protecting against chemicals, The type of protective equipment must be selected according to the concentration and amount of the dangerous substance at the specific workplace.|Eye protection: Face shield and safety glasses Use equipment for eye protection tested and approved under appropriate government standards such as NIOSH (US) or EN 166(EU).|Hand protection: Handle with gloves. Gloves must be inspected prior to use. Use proper glove removal technique (without touching glove's outer surface) to avoid skin contact with this product. Dispose of contaminated gloves after use in accordance with applicable laws and good laboratory practices. Wash and dry hands.|Respiratory protection: Where risk assessment shows air-purifying respirators are appropriate use a full-face particle respirator type N100 (US) or type P3 (EN 143) respirator cartridges as a backup to engineering controls. If the respirator is the sole means of protection, use a full-face supplied air respirator. Use respirators and components tested and approved under appropriate government standards such as NIOSH (US) or CEN (EU).|PRECAUTIONS FOR "CARCINOGENS": ... Dispensers of liq detergent /should be available./ ... Safety pipettes should be used for all pipetting. ... In animal laboratory, personnel should ... wear protective suits (preferably disposable, one-piece & close-fitting at ankles & wrists), gloves, hair covering & overshoes. ... In chemical laboratory, gloves & gowns should always be worn ... however, gloves should not be assumed to provide full protection. Carefully fitted masks or respirators may be necessary when working with particulates or gases, & disposable plastic aprons might provide addnl protection. ... Gowns ... /should be/ of distinctive color, this is a reminder that they are not to be worn outside the laboratory. /Chemical Carcinogens/

... Can be totally destroyed by drastic treatment such as autoclaving ... or by treatment with hypochlorite.|PRECAUTIONS FOR "CARCINOGENS": A high-efficiency particulate arrestor (HEPA) or charcoal filters can be used to minimize amt of carcinogen in exhausted air ventilated safety cabinets, lab hoods, glove boxes or animal rooms ... Filter housing that is designed so that used filters can be transferred into plastic bag without contaminating maintenance staff is avail commercially. Filters should be placed in plastic bags immediately after removal ... The plastic bag should be sealed immediately ... The sealed bag should be labelled properly ... Waste liquids ... should be placed or collected in proper containers for disposal. The lid should be secured & the bottles properly labelled. Once filled, bottles should be placed in plastic bag, so that outer surface ... is not contaminated ... The plastic bag should also be sealed & labelled. ... Broken glassware ... should be decontaminated by solvent extraction, by chemical destruction, or in specially designed incinerators. /Chemical Carcinogens/

PRECAUTIONS FOR "CARCINOGENS": Smoking, drinking, eating, storage of food or of food & beverage containers or utensils, & the application of cosmetics should be prohibited in any laboratory. All personnel should remove gloves, if worn, after completion of procedures in which carcinogens have been used. They should ... wash ... hands, preferably using dispensers of liq detergent, & rinse ... thoroughly. Consideration should be given to appropriate methods for cleaning the skin, depending on nature of the contaminant. No standard procedure can be recommended, but the use of organic solvents should be avoided. Safety pipettes should be used for all pipetting. /Chemical Carcinogens/|PRECAUTIONS FOR "CARCINOGENS": In animal laboratory, personnel should remove their outdoor clothes & wear protective suits (preferably disposable, one-piece & close-fitting at ankles & wrists), gloves, hair covering & overshoes. ... Clothing should be changed daily but ... discarded immediately if obvious contamination occurs ... /also,/ workers should shower immediately. In chemical laboratory, gloves & gowns should always be worn ... however, gloves should not be assumed to provide full protection. Carefully fitted masks or respirators may be necessary when working with particulates or gases, & disposable plastic aprons might provide addnl protection. If gowns are of distinctive color, this is a reminder that they should not be worn outside of lab. /Chemical Carcinogens/|PRECAUTIONS FOR "CARCINOGENS": ... Operations connected with synth & purification ... should be carried out under well-ventilated hood. Analytical procedures ... should be carried out with care & vapors evolved during ... procedures should be removed. ... Expert advice should be obtained before existing fume cupboards are used ... & when new fume cupboards are installed. It is desirable that there be means for decreasing the rate of air extraction, so that carcinogenic powders can be handled without ... powder being blown around the hood. Glove boxes should be kept under negative air pressure. Air changes should be adequate, so that concn of vapors of volatile carcinogens will not occur. /Chemical Carcinogens/|PRECAUTIONS FOR "CARCINOGENS": Vertical laminar-flow biological safety cabinets may be used for containment of in vitro procedures ... provided that the exhaust air flow is sufficient to provide an inward air flow at the face opening of the cabinet, & contaminated air plenums that are under positive pressure are leak-tight. Horizontal laminar-flow hoods or safety cabinets, where filtered air is blown across the working area towards the operator, should never be used ... Each cabinet or fume cupboard to be used ... should be tested before work is begun (eg, with fume bomb) & label fixed to it, giving date of test & avg air-flow measured. This test should be repeated periodically & after any structural changes. /Chemical Carcinogens/|For more Preventive Measures (Complete) data for AFLATOXIN G1 (9 total), please visit the HSDB record page.

PRECAUTIONS FOR "CARCINOGENS": Procurement ... of unduly large amt ... should be avoided. To avoid spilling, carcinogens should be transported in securely sealed glass bottles or ampoules, which should themselves be placed inside strong screw-cap or snap-top container that will not open when dropped & will resist attack from the carcinogen. Both bottle & the outside container should be appropriately labelled. ... National post offices, railway companies, road haulage companies & airlines have regulations governing transport of hazardous materials. These authorities should be consulted before ... material is shipped. /Chemical Carcinogens/|PRECAUTIONS FOR "CARCINOGENS": When no regulations exist, the following procedure must be adopted. The carcinogen should be enclosed in a securely sealed, watertight container (primary container), which should be enclosed in a second, unbreakable, leakproof container that will withstand chem attack from the carcinogen (secondary container). The space between primary & secondary container should be filled with absorbent material, which would withstand chem attack from the carcinogen & is sufficient to absorb the entire contents of the primary container in the event of breakage or leakage. Each secondary container should then be enclosed in a strong outer box. The space between the secondary container & the outer box should be filled with an appropriate quantity of shock-absorbent material. Sender should use fastest & most secure form of transport & notify recipient of its departure. If parcel is not received when expected, carrier should be informed so that immediate effort can be made to find it. Traffic schedules should be consulted to avoid ... arrival on weekend or holiday ... /Chemical Carcinogens/

May be fatal if inhaled. May cause respiratory tract irritation. May be fatal if absorbed through skin. May cause skin irritation. May cause eye irritation. May be fatal if swallowed.

Aspergillus strains were isolated from municipal solid waste compost from a municipal solid waste composting plant in Grenoble France cultured on sucrose yeast extract medium; mycotoxin quantification 40 ug/L. Aflatoxon G1 produced by A. parasiticus was recovered from the first stage of composting(1).

most toxic

LD50 Rat intraperitoneal 14,900 ug/kg

/AQUATIC SPECIES/ Exposure of Rana temporaria tadpoles to aflatoxin G1 at 0.25 ug/mL induced limb abnormalities similar to those caused by thalidomide in human fetuses.|/AQUATIC SPECIES/ Groups of Trout were administered 0 (control), 4 ppb aflatoxin B1, 8 ppb aflatoxin B1, and 20 ppb aflatoxin G1 in diet, 20-57/group. The incidence of liver hepatomas at 12 months was 0/20, 10/40 (P< 0.05), 40/57 (P< 0.0001), 1/20 (no significance). At 16 months, the incidence of liver hepatomas was 0/40, 14/40 (P< 0.0001), 32/20 (P< 0.0001), and 7/40 (P< 0.05).

Aflatoxin G1 is a toxic metabolite of the fungi Aspergillus flavus and A. parasiticus(1).

TERRESTRIAL FATE: Based on a classification scheme(1), a Koc range of 682 to 2.3X10+4 for analogous aflatoxin B1(2), indicates that aflatoxin G1 is expected to have low to no mobility in soil(SRC). Volatilization of aflatoxin G1 from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 5.0X10-13 atm-cu m/mole(SRC), using a fragment constant estimation method(3). Aflatoxin G1 is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 5.9X10-11 mm Hg at 25 °C(SRC), determined from a fragment constant method(4).|AQUATIC FATE: Based on a classification scheme(1), a Koc range of 682 to 2.3X10+4 for analogous aflatoxin B1(2), indicates that aflatoxin G1 is expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(3) based upon an estimated Henry's Law constant of 5.0X10-13 atm-cu m/mole(SRC), developed using a fragment constant estimation method(4). According to a classification scheme(6), an estimated BCF of 3(SRC), from an estimated log Kow of 0.50(6) and a regression-derived equation(7), suggests the potential for bioconcentration in aquatic organisms is low(SRC).|ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), aflatoxin G1, which has an estimated vapor pressure of 5.9X10-11 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 aflatoxin G1 may be removed from the air by wet and dry deposition(SRC). Aflatoxin G1 absorbs UV light at wavelengths of 243, 257 and 362 nm(3) and, therefore, may be susceptible to direct photolysis by sunlight(SRC).

The aflatoxins may undergo hydrolysis in the environment as they contain a cyclic ester functionality that hydrolyze under environmental conditions(1). Rates may be similar to non-cyclic esters, which are in the range of months to years time frame; however, steric hindrance and ring strain effects may be important(2). Aflatoxin G1 absorbs UV light at wavelengths of 243, 257 and 362 nm(3) and, therefore, may be susceptible to direct photolysis by sunlight(SRC).

An estimated BCF of 3 was calculated in fish for aflatoxin G1(SRC), using an estimated log Kow of 0.50(1) and a regression-derived equation(2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organisms is low(SRC).

Koc values of 23170, 1570 and 682 were calculated(SRC) from Freundlich's adsorption coefficients of 238.49, 76.19 and 17.40 mg/kg soil, respectively, for analogous aflatoxin B1 in a silty clay loam (pH 7.3, 0.597% organic matter, CEC /cation exchange capacity/ of 18.0 cmol/kg), a silt loam (pH 5.8, 2.818% organic matter, CEC of 11.7 cmol/kg) and a sandy loam (pH 6.0, 1.478% organic matter, CEC of 5.4 cmol/kg), respectively(1). According to a classification scheme(2), these Koc values suggest that the aflatoxins may range in mobility from low to immobile depending on the soil. Cation exchange capacity was positively correlated with the adsorption coefficient value(1). In addition, the type of clay (2:1 expanding clays were found in the silty clay loam) appears to influence the amount of adsorption to soil(1).

The Henry's Law constant for aflatoxin G1 is estimated as 5.0X10-13 atm-cu m/mole(SRC) using a fragment constant estimation method(1). This Henry's Law constant indicates that aflatoxin G1 is expected to be essentially nonvolatile from water and moist soil surfaces(2). Aflatoxin G1 is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 5.9X10-11 mm Hg(SRC), determined from a fragment constant method(3).

Commercially available market basket samples were collected in Tokyo, Japan during 1986 to 1990; aflatoxin concentrations were determined in 3054 samples (803 samples of cereals, 540 samples of nuts, 540 samples of beans, 564 samples of spices, and 607 samples of other foods)(1).|Aflatoxin G1 concentrations of

Three groups of four Large White sows were fed diets containing either 800 ppb purified aflatoxin B1 (group 1), 800 ppb purified aflatoxin G1 (group 2) or 400 ppb B1 and 400 ppb G1 (group 3) throughout gestation and lactation. A control group of four sows was fed a diet free of aflatoxins. Aflatoxins B1 and M1 were found in milk samples taken five and 25 days after parturition from the sows of group 1, aflatoxin G1 was present in the milk of the sows of group 2 and all three aflatoxins were present in samples from the sows of group 3. The concentration of aflatoxin in the milk was about 1000-fold lower than that in the feed, but increased over the 25 days after parturition.

Monitoring data indicate that the general population may be exposed to aflatoxin G1 via ingestion of contaminated foods. (SRC)

Aflatoxins B1 & G1 & their metabolites exist in systemic blood as protein conjugates. This conjugation is specific to plasma albumin & proceeds enzymatically by liver & kidney cells. The albumin-aflatoxin conjugate is permanent & conjugation is an irreversible one.|Three groups of four Large White sows were fed diets containing either 800 ppb purified aflatoxin B1 (group 1), 800 ppb purified aflatoxin G1 (group 2) or 400 ppb B1 and 400 ppb G1 (group 3) throughout gestation and lactation. A control group of four sows was fed a diet free of aflatoxins. Aflatoxins B1 and M1 were found in milk samples taken five and 25 days after parturition from the sows of group 1, aflatoxin G1 was present in the milk of the sows of group 2 and all three aflatoxins were present in samples from the sows of group 3. The concentration of aflatoxin in the milk was about 1000-fold lower than that in the feed, but increased over the 25 days after parturition.

Yields aflatoxin B3 in rhizopus ... yields aflatoxin gm1 in rat. From table/|Aflatoxin B1, aflatoxin B2, & aflatoxin G1 admin iv to rats were rapidly metabolized to 7 groups of metabolites each, 6 of which were excreted in the bile. All 3 toxins were hydroxylated at the 2- & 4-positions. Bile from the rats that had received aflatoxin G1 contained glucuronide.|...The incubation of human liver microsomes with aflatoxin B1 /or/ aflatoxin G1 ...yielded genotoxic metabolites that induced umuC gene expression in Salmonella typhimurium (TA-1535/psK1002). The rank order of genotoxic potency was ...aflatoxin B1>aflatoxin G1. Microsomal activation of the ...aflatoxins was completely inhibited upon incubation with polyclonal antibodies against p450NF, and immunochemical determinations of p450NF /(nifedipine oxidase)/ in the liver microsomal preparations were correlated with the microsomal activation of ...aflatoxin G1 and aflatoxin B1. P450NF converted the ...aflatoxins to genotoxic metabolites in a reconstituted monooxygenase system containing the purified enzyme and an NADPH generating system. ...

Ability of aflatoxin B1, aflatoxin B2, & aflatoxin G1 to inhibit RNA polymerase activity & decr RNA content in rat hepatocyte nuclei was qualitatively similar to the carcinogenic & acute & subacute toxic actions of these compounds. Aflatoxin g1 induced a rapid macrosegregation of the fibrillar & granular portions of the hepatocyte nucleolus.|In vitro studies with human liver indicate that the major catalyst involved in the bioactivation of the hepato-carcinogen aflatoxin B1 to its genotoxic 2,3-epoxide derivative is cytochrome P-450NF, a previously characterized protein that also catalyzes the oxidation of nifedipine and other dihydropyridines, quinidine, macrolide antibiotics, various steroids, and other compounds. ...Cytochrome p-450NF or a closely related protein also appears to be the major catalyst involved in the activation of aflatoxin G1 and sterigmatocystin, the latter compound being more genotoxic than aflatoxin B1 in these systems. Several drugs and conditions are known to influence the levels and activity of cytochrome p-450NF in human liver, and the activity of the enzyme can be estimated by noninvasive assays. These findings provide a test system for the hypothesis that a specific human disease state (liver cancer) is linked to the level of oxidative metabolism in populations in which aflatoxin ingestion is high.|Aflatoxin B1, aflatoxin G1 & aflatoxin G2 inhibited incorporation of (14)carbon labeled orotic acid into the RNA of rat liver slices at toxin concentrations of 100 umole/3 mL. Respective percent inhibitions were approx 90, 40, & 20. Aflatoxin B1, 20 umole/3 mL, aflatoxin G1, 150 umole/3 mL, & aflatoxin G2, 230 umole/3 mL inhibited the incorporation of (14)carbon labeled dl-leucine into proteins of rat liver slices by 32%, 35%, & 38%, respectively.|Phagocytosis, intracellular killing of Candida albicans, and superoxide production by rat peritoneal macrophages exposed to aflatoxins B1, B2, G1, G2, B2a, and M1 at several times and concn were analyzed to evaluate the intensity of a depressive effect for each mycotoxin. All aflatoxins used at very low concn had a depressive effect on the functions of macrophages. The biggest impairment of phagocytosis, intracellular killing, and spontaneous superoxide production was observed in macrophages exposed to aflatoxins B1 and M1.|Among the toxic aflatoxins, aflatoxins B1 and G1 are the most biologically active, but other derivatives also exhibit carcinogenicity. Aflatoxin B1 requires metabolic activation by the cytochrome p450 dependent mixed-function oxidase to be converted to the reactive 2,3-epoxide, the ultimate carcinogen. The aflatoxins, eg, aflatoxin B1, are genotoxic carcinogens and the reactive metabolites react with DNA. The major adduct formed with DNA in intracellular reactions is formed from the 2-position of aflatoxin B1 and the N-7 position of guanine in DNA.

Carcinogens, Mutagens, Teratogens

/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/

/HUMAN EXPOSURE STUDIES/ There are four generally recognized aflatoxins, B1, B2, G1, & G2. Although they are generally associated with aspergillus flavus, many other Aspergillus species & also members of the Penicillium & Rhizopus genera can also produce the carcinogens. This means that a range of both animal & human foodstuffs & not just the major source, peanuts, can become contaminated with aflatoxin. There is clearly the possibility of a real hazard to man since the first criterion, the presence of the carcinogen in the diet, has been established.|/EPIDEMIOLOGY STUDIES/ To find out if the presumed intake of dietary aflatoxins (AFB1 and AFG1) has adverse effect on the liver of Ghanaians, the toxins were measured in serum, urine and fecal specimens obtained from a group of apparently healthy Ghanaian adults. Liver status of the subjects was monitored with serum alpha fetoprotein (AFP), alpha-l-antitrypsin (AAT) and direct: total bilirubin ratio. Aflatoxin G1, AFB1 and AFQ1, AFM1 (both metabolites of AFB1) were detected in one or more of the body specimens in 35% of the subjects (AFB1+ group). Sixty-five percent (26 out of 40) of the subjects had only AFG1 in their body specimens (AFB1- group). Serum levels of AFP (greater than 20.0 ng/mL, AAT (greater than 170.0 mg/dL) and direct: total bilirubin ratio (greater than 0.5) which indicate absence of predisposition to liver cancer in all the subjects but suggestive of liver inflammation were noted in both the AFB1+ and AFB1- subjects. The pattern of distribution of the aflatoxins in the subjects suggests that the suspected liver inflammation may involve other factors and may not only be due to the present intake levels of aflatoxins.|/ALTERNATIVE and IN VITRO TESTS/ Pregnane X receptor (PXR) is a member of the nuclear hormone receptor (NHR) superfamily, which regulates xenobiotic and endobiotic metabolism in the liver. This transcription factor is activated by structurally diverse ligands, including drugs and environmental pollutants. PXR regulates the expression of numerous genes that function in biotransformation and the disposition of xenobiotics upon binding to an AG(G/T)TCA DNA motif in target promoter regions. /Investigators/ performed a screen of mycotoxins that pose a known environmental threat to human and animal health for the ability to activate PXR function in a human hepatocyte cell line, HepG2. /Investigators/ found that aflatoxins B1, M1, and G1 activated PXR. This activation was associated with upregulation of CYP3A4 expression and increased occupancy of PXR protein on the CYP3A4 promoter. Using a microarray approach, /investigators/ also found that aflatoxin B1 upregulated the expression of multiple genes involved in xenobiotic metabolism, including genes known to be regulated in a PXR-dependent fashion. /The investigators/ also observed an effect of aflatoxin B1 on the expression in other functional groups of genes, including the downregulation of genes involved in cholesterologenesis. The results of this study indicate that aflatoxin B1 is able to activate PXR, a known regulator of liver xenobiotic metabolism, in human hepatocytes, and it can upregulate the expression of PXR-dependent genes responsible for aflatoxin B1 biotransformation, including CYP3A4.|/IMMUNOTOXICITY/ /The objective of this study was/ to explore the effect of AFG1 on the expression of human leukocyte antigen (HLA-I) molecule in human esophageal epithelial cells. Western Blot and RT-PCT analysis was used to explore the effect of AFG1 on the antigen presenting function of primary cultured esophageal epithelial cells. The protein expression of HLA-ABC was significantly decreased in the groups treated with 100, 1000 and 2000 ug/L AFG1 as compared with the solvent control group (P < 0.05). Within the range of 100 - 2000 ug/L AFG1, the protein expression level of HLA-ABC of esophageal epithelial cells decreased gradually, and showed significant negative correlation (r = -0.921, n = 3, P < 0.01). The effect of AFG1 on the expression of HLA-ABC mRNA was further confirmed by RT-PCR analysis. The results showed that after treated with 100 ug/L, 1000 ug/L and 2000 ug/L AFG1, the expression of HLA-A mRNA was decreased significantly as compared with the solvent control (P < 0.05), and the expression of HLA-B mRNA was decreased in the 2000 ug/L AFG1 treated group (P < 0.05), while there was no effect on the expression of HLA-C mRNA...|For more Human Toxicity Excerpts (Complete) data for AFLATOXIN G1 (10 total), please visit the HSDB record page.

aflatoxin G(1)

Aflatoxins are produced primarily by the common fungus Aspergillus flavus and the closely related species A. parasiticus. These are well defined species: A. flavus produces only B aflatoxins and sometimes the mycotoxin cyclopiazonic acid (CPA), while A. parasiticus produces both B and G aflatoxins, but not CPA. Aflatoxin M1 is a metabolite of aflatoxin B1 that can occur in milk and milk products from animals consuming feed contaminated with B aflatoxins.|Of the four major aflatoxins (B1, G1, B2, G2), B1 is the most potent and most common. Whenever they occur as food contaminants, aflatoxin B1 always is present. The other major aflatoxins have not been reported in the absence of B1. Aflatoxins are densely fluorescent; the B refers to blue, while the G signifies green fluorescence.

UV spectrophotometric & fluorescence spectrophotometric investigations were performed on aflatoxins B1 & G1 with aim of their unequivocal identification & quantitative estimation. Lower limits of quantitative & semiquantitative estimations for G1 were 1 ug/mL using UV spectrophotometry & 0.3 ng using thin layer chromatograph (semiquantitative).|A reliable and rapid method has been developed for the determination of 10 mycotoxins (beauvericin, enniatin A, A1, B1, citrinin, aflatoxin B1, B2, G1, G2 and ochratoxin A) in eggs at trace levels. Ultra-high-pressure liquid chromatography coupled to tandem mass spectrometry (UHPLC-MS/MS) has been used for the analysis of these compounds in less than 7 min. Mycotoxins have been extracted from egg samples using a QuEChERS-based extraction procedure (Quick, Easy, Cheap, Effective, Rugged and Safe) without applying any further clean-up step. Extraction, chromatographic and detection conditions were optimised in order to increase sample throughput and sensitivity. Matrix-matched calibration was used for quantification. Blank samples were fortified at 10, 25, 50 and 100 ug kg(-1), and recoveries ranged from 70% to 110%, except for ochratoxin A and aflatoxin G1 at 10 ug kg(-1), and aflatoxin G2 at 50 ug kg(-1). Relative standard deviations were lower than 25% in all the cases. Limits of detection ranged from 0.5 ug kg(-1) (for aflatoxins B1, B2 and G1) to 5 ug kg(-1) (for enniatin A, citrinin and ochratoxin A) and limits of quantification ranged from 1 ug kg(-1) (for aflatoxins B1, B2 and G1) to 10 ug kg(-1) (for enniatin A, citrinin and ochratoxin A). Seven samples were analyzed and aflatoxins B1, B2, G1, G2, and beauvericin were detected at trace levels.|A high-performance liquid chromatographic method with on-line post-column photochemical derivatization and fluorimetric detection for the simultaneous separation and quantitative determination of aflatoxin (AF) B(1), B(2), G(1), and G(2) in foodstuffs and feed materials is reported. The chromatographic separation is accomplished by using a C(18) column eluted with an isocratic mobile phase consisting of water, methanol, and acetonitrile. The sample preparation requires a simple extraction of aflatoxins with a mixture of water and methanol, and a purification step by immunoaffinity column clean-up. The total analysis time, including sample preparation and chromatographic separation, does not exceed 40 min with a run time of 10 min. The procedure for the determination of aflatoxins in food samples and cereals for animal consumption has been extensively validated, in agreement with Regulation (EC) No. 882/2004, demonstrating the conformity of the method with provisions of Regulation (EC) No. 401/2006 in terms of sensitivity, linearity, selectivity, and precision.|Efficient detection of aflatoxins B1, B2, G1, and G2 has been performed by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry using a UV-absorbing ionic liquid matrix to obtain "matrix-free" mass spectra and addition of NaCl to enhance sensitivity via Na+ cationization. Using ionic alpha-cyano-4-hydroxycinnamic acid (Et3N-alpha-CHCA) as the matrix, matrix-free mass spectra in the m/z range of interest are acquired, and the B1, B2, G1, and G2 aflatoxins are readily detected with an LOD as low as 50 fmol. The technique is fast, requires little sample preparation and no derivatization or chromatographic separation, and seems therefore to be suitable for high-throughput aflatoxin screening. It should be easily extended to other micotoxins and provide an attractive technique to control the quality of major crops subjected to huge world commercial trades such as peanuts, corn, and rice as well as to monitor bioterrorism threats by micotoxin poisoning.|For more Analytic Laboratory Methods (Complete) data for AFLATOXIN G1 (22 total), please visit the HSDB record page.

An HPLC method for determining aflatoxins (B1, B2, G1, G2, M1) using a radial compression separation system is presented. Spiked samples of liver, serum, & urine showed good resolution of all aflatoxins peaks at the higher flow rates.|Aflatoxins B2, G1, G2, & M1 & aflatoxicol were recovered from human serum using hexane-chloroform extraction with mean recoveries ranging from 67.3-81.2%. Detection limits ranged from 25-500 pg/mL. Quantitation was by high pressure liquid chromatography using fluorescence detector.|Modification of a reverse-phase HPLC procedure permitted the determination of the parent aflatoxins & various metabolites in animal tissues. Trifluoroacetic acid catalyzed the conversion of aflatoxin G1, B1, M1 & Q1 to the fluorescent derivatives G2a, B2a, M2a, & Q2a.|Human urine and methanol extracted tissues and sputum were examined. Trichothecenes were tested using competitive ELISA techniques. Aflatoxins B1, B2, G1, and G2, and ochratoxin A were tested by using immunoaffinity columns and fluorometry. Test sensitivity and specificity were determined. Levels of detection for the various mycotoxins varied from 0.2 ppb for trichothecenes, 1.0 ppb for aflatoxins, and 2.0 ppb for ochratoxins. Trichothecene levels varied in urine, sputum, and tissue biopsies (lung, liver, brain) from undetectable (<0.2 ppb) to levels up to 18 ppb. Aflatoxin levels from the same types of tissues varied from 1.0 to 5.0 ppb. Ochratoxins isolated in the same type of tissues varied from 2.0 ppb to > 10.0 ppb. Negative control patients had no detectable mycotoxins in their tissues or fluids. These data show that mycotoxins can be detected in body fluids and human tissue from patients exposed to mycotoxin producing molds in the environment, and demonstrate which human tissues or fluids are the most likely to yield positive results.

Health Hazards -> Carcinogens, Mutagens, Teratogens

Food Contaminant -> MYCOTOXIN;