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How the carcinogenic aflatoxin produce?

Posted on November 11, 2019 by Josephine
How the carcinogenic aflatoxin produce?

There is a risk of aflatoxin contamination in many foods. It is more toxic than arsenic, which can cause acute poisoning, and even cancer and death. What are the conditions for aflatoxin production? The following is a small series of references to introduce some relevant knowledge.

Aflatoxin is a see also of mycotoxin that is a group of compounds with a similar chemical structure. The basic structure of aflatoxin is difuran ring and coumarin. B1 is a derivative of dihydrofuran oxaphthalene, which contains a difuran ring and oxygen. The former is a basic toxic structure. The latter is related to carcinogenesis. M1 is a metabolite derived from aflatoxin B1 by hydroxylation in the body. The main molecular form of aflatoxin contains B1, B2, G1, G2, M1, M2, etc. In the aflatoxin, M1 and M2 are mainly present in milk. B1 is the most toxic and carcinogenic substance.

The optimum temperature for the growth of Aspergillus flavus is 26 ° C - 28 ° C. The higher the temperature is, the faster the growth of Aspergillus flavus is. With the temperature of 28 ° C to 33 ° C and the humidity of 80% - 90% in the environment, mold can quickly secrete toxins. So, this toxin can survive in the high temperature and very humid south. Besides, these molds also like to grow in nuts and oily seeds, so they are also easy to contaminate grains like corn, figs, and cereals. Therefore we can often see the aflatoxin peanuts and the aflatoxin corn. The simplest method of detection is to use an aflatoxin tester.

After aflatoxin enters the body, it is mainly metabolized under the action of hepatocyte endoplasmic reticulum microsomal mixed-function oxidase system. Aflatoxin is not carcinogenic without metabolic activation.

Aflatoxin is a toxic substances thatmuch more toxic than cyanide, arsenide and organic pesticides with B1 being the most toxic. When a person consumes a large amount, acute poisoning, acute hepatitis, hemorrhagic necrosis, hepatic steatosis, and bile duct hyperplasia may occur.

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