1165-39-5 Usage
Chemical Properties
Different sources of media describe the Chemical Properties of 1165-39-5 differently. You can refer to the following data:
1. yellow powder
2. The aflatoxins are a group of molds produced by the fungus Aspergillus flavus. They are natural contaminants of fruits, vegetables, and grains. They are also described as a series of condensed ring heterocyclic compounds. They form colorless to pale yellow crystals. Practically insoluble in water.
Uses
Different sources of media describe the Uses of 1165-39-5 differently. You can refer to the following data:
1. Aflatoxins B1, B2, G1, G2 as secondary metabolites of fungal species such as Aspergillus flavus or Aspergillus parasiticus growing on a variety of foods (peanuts, nuts, spices, cereals). Aflatoxins a
re a group of very carcinogenic mycotoxins with hepatotoxic effects.
2. Aflatoxin G1 is the major analogue of the green fluorescent family of bisfuranocoumarin mycotoxins produced by Aspergillus flavus and related species. Alfatoxins are one of the most potent mycotoxins known but are in fact "pre-toxins", requiring metabolic activation to the toxic principle. Aflatoxins are found widely in nature in trace amounts, particularly in grains and nuts. The toxicity of these metabolites was first recognised in the 1950s and their structures elucidated in 1963. Aflatoxins have been extensively reviewed.
3. Aflatoxin G1 from Aspergillus flavus has been used as a standard for the determination of aflatoxin in various samples.
General Description
Certan Vial
Biochem/physiol Actions
Hepatocarcinogen. Food contaminant produced by Aspergillus flavus, a common soil fungus.
Safety Profile
Confirmed human carcinogen with experimental carcinogenic and neoplastigenic data. Poison by ingestion and intraperitoneal routes. Mutation data reported. When heated to decomposition it emits acrid smoke and irritating fumes. See also various aflatoxins
Potential Exposure
Aflatoxins are a group of toxic metabolites produced by certain types of fungi. Aflatoxins are not commercially manufactured; they are naturally occurring contaminants that are formed by fungi on food during conditions of high temperatures and high humidity. Most human exposure to aflatoxins occurs through ingestion of contaminated food. The estimated amount of aflatoxins that Americans consume daily is estimated to be 0.15 0.50 μg. Grains, peanuts, tree nuts, and cottonseed meal are among the more common foods on which these fungi grow. Meat, eggs, milk, and other edible products from animals that consume aflatoxincontaminated feed may also contain aflatoxins. Aflatoxins can also be breathed in
Shipping
UN3172 Toxins, extracted from living sources, solid or liquid, Hazard Class: 6.1; Labels: 6.1-Poisonous materials, Technical Name Required. UN2811 Toxic solids, organic, n.o.s., Hazard Class: 6.1; Labels: 6.1-Poisonous materials, Technical Name Required.
Incompatibilities
Incompatible with oxidizers (chlorates, nitrates, peroxides, permanganates, perchlorates, chlorine, bromine, fluorine, etc.); contact may cause fires or explosions. Keep away from alkaline materials, strong bases, strong acids, oxoacids, epoxides.
Waste Disposal
Consult with environmental regulatory agencies for guidance on acceptable disposal practices. Generators of waste containing this contaminant (≥100 kg/mo) must conform with EPA regulations governing storage, transportation, treatment, and waste disposal. Use of oxidizing agents, such as hydrogen peroxide or 5% sodium hypochlorite bleach. Acids and bases may also be used.
Check Digit Verification of cas no
The CAS Registry Mumber 1165-39-5 includes 7 digits separated into 3 groups by hyphens. The first part of the number,starting from the left, has 4 digits, 1,1,6 and 5 respectively; the second part has 2 digits, 3 and 9 respectively.
Calculate Digit Verification of CAS Registry Number 1165-39:
(6*1)+(5*1)+(4*6)+(3*5)+(2*3)+(1*9)=65
65 % 10 = 5
So 1165-39-5 is a valid CAS Registry Number.
1165-39-5Relevant articles and documents
Quantitative carcinogenesis and dosimetry in rainbow trout for aflatoxin B1 and aflatoxicol, two aflatoxins that form the same DNA adduct
Bailey, George S.,Loveland, Patricia M.,Pereira, Cliff,Pierce, Donald,Hendricks, Jerry D.,Groopman, John D.
, p. 25 - 38 (1994)
Two exposure protocols were used to establish complete dose-response relationships for the hepatic carcinogenicity and DNA adduction in vivo of aflatoxin B1 (AFB1) and aflatoxicol (AFL) in rainbow trout. By passive egg exposure, AFL was taken up less than AFB1, but was more efficiently sequestered into the embryo itself, to produce an embryotic DNA binding curve that was linear with carcinogen dose and with a DNA binding index three-fold greater than AFNB1. Both aflatoxins produced the same phenotypic respone, predominantly mixed hepatocellular/cholangiocelllular carcinoma. Tumor responses as logit vs. ln were parallel-offset, non-linear response showing a three-fold greater carcinogenic potency of AFL at all doses examined (i.e. 3 times more AFB1 than AFL required to produce an equivalent liver tumor incidence). By molecular dosimetry analysis (logit vs. ln ), the two data sets were coincident, indicating that, per DNA adduct formed in vivo in total embryonic DNA, these two aflatoxins were equally efficient in tumor initiation. By dietary fry exposure, both carcinogens produced linear DNA binding dose response in liver, but with an AFL target organ DNA binding index only 1.14 times of that of AFB1 by this exposure route. The tumor dose-response curves also did not exhibit the three-fold difference shown by embryo exposure, but very closely positioned non-linear curves. Since the DNA binding indices differed by only 14 percent, the resulting molecular dosimetry curves for AFL and AFB1 by dietary exposure were similar to the tumor response curves. These results indicate that differing exposure routes produced differing relative carcinogenicity estimates based on doses applied, as a result of protocol-dependent differences in AFL and AFB1 pharmacokinetic behaviors, but that potency comparisons based on molecular dose receiving were similar for the two protocols. By comparison with standard DNA adducts produced in vitro using the dimethyloxirane-produced 8,9-epoxides of AFB1 and AFL, we conclude that >99 percent of AFL-DNA adducts produced in vivo were identical to those produced by AFB1. Thus similar molecular dosimetry responses should be expected under all exposure protocols in which the two parent carcinogens do not exhibit differing toxicities to the target organ. - Keywords; Aflatoxin B1; Aflatoxicol; Molecular dosimetry; Hepatocarcinogenesis; Rainbow trout; DNA adducts
