The Nature of ochratoxin

Posted by beauty33 on November 15th, 2021

Physical and chemical properties

OTA was first purified by VanderMerwe et al. (1965) from the culture of Aspergillus ochraccus (According to Marquardt and Frohlich, 1992, it was reported that the bacterium is now called A. alutaceus). Wei Runyun et al. (1981) and Sun Huilan et al. (1989) also proposed pure OTA products from grain and compound feed respectively. Analysis shows that OTA is composed of 7-carboxy-5-chloro-8-hydroxy-3,4-dihydro-R-methylisocoumarin (abbreviated as Oa) and L-β-phenylalanine connected by peptide bonds. Into (see the chemical structure of ochratoxin A), molecular formula: C20H18CINO6, molecular weight 403.

OTB is a dechlorinated derivative of OTA, and OTC is an ethyl ester of OTA. OTA is a colorless crystal, soluble in organic solvents (chloroform and methanol) and dilute sodium bicarbonate solution, slightly soluble in water. OTA and OTB show green and blue fluorescence under ultraviolet irradiation, and the maximum absorption peaks are 333nm and 318nm, respectively.

Toxicity

The toxicity of ochratoxin A to animals and humans mainly includes kidney toxicity, liver toxicity, teratogenic, carcinogenic, mutagenic and immunosuppressive effects. After entering the body, ochratoxin A is converted into 4-hydroxy ochratoxin A and 8-hydroxy ochratoxin A under the action of liver microsomal mixed function oxidase, of which 4-hydroxy ochratoxin A is the main component. .

The order of the toxicity of ochratoxin is: OTA>OTC>OTB. This largely depends on the ionization constant of the eighth hydroxyl group in the molecule. The content of OTB and OTC in contaminated feed is generally lower, and it is less toxic to most animals than OTA. Therefore, it is not necessary to consider the feed test, and mainly analyze the OTA content. Recently, Creppy et al. (1983) and Hadidane et al. (1992) replaced phenylalanine in OTA molecules with amino acids such as tryptophan, valine, and lysine, and obtained a series of OTA analogues. Substitution analogs of amino acid, threonine and alanine are the most toxic, followed by substitution analogs of methionine, tryptophan and glutamate, and substitution analogs of glutamine and proline have the lowest toxicity. Hadidane et al. (1991) reported that threonine, hydroxyproline and lysine substitution analogues of OTA also exist in nature.

The investigation of Marquardt et al. (1992) showed that when the content of OTA in the feed is 0.3-16mg/kg, it can cause poisoning of livestock and poultry, and increase the mortality rate by 2% to 58%. Madsen et al. (1982) reported that continuous feeding of 200μg/kg of OTA for 4 months had little effect on pigs, and when the OTA content was greater than 1400μg/kg, it significantly reduced the feed intake and growth rate of pigs, and the amount of water consumed. Increase. Huff et al. (1974) reported that continuous feeding of feed containing 0.5 to 1.0 mg/kg OTA for 3 weeks had no effect on the weight gain of broiler chickens, while continuous feeding of feed containing 0.5 mg/kg OTA for 6 weeks could reduce laying hens’ Egg production performance and feed conversion rate.

Dwivedi and Burns (1985) reported that OTA can cause changes in the immune organs of livestock and poultry, reducing the number of white blood cells in the thymus, bursa of Fabricius, spleen and lymph nodes, and the migration of macrophages and monocytes. From the data of Lee et al. (1989), it seems that it can also inhibit the activity of cellular immunity (T cells and B cells).

Appelgren and Arora (1983), Kovasf and Vanyl (1994) reported that OTA can have teratogenic effects on the fetus through the placenta, but pigs are not very sensitive to it. Research on the carcinogenic effects of OTA is still at the stage of experimental animals, and there is no report on livestock and poultry. Krogh (1991) reported that blood total protein, albumin and globulin content, and renal phosphoenolpyruvate carboxykinase (PEPCK) activity can be used as sensitive indicators of OTA poisoning.

Many studies have been conducted on the poisoning mechanism of OTA. Endou et al. (1984) reported that OTA can inhibit the anion transport system of renal proximal tubule epithelial cells, and make alanine aminopeptidase and leucine aminopeptidase in the urine. (1euineaminopeptidase) increased in concentration. Meisner et al. (1983, 1986) successively proved that OTA can inhibit the activity of renal PEPCK, thereby inhibiting renal glucose production, but the method of inhibition of OTA is still inconclusive. Creppy et al. (1983) reported that OTA is also a competitive inhibitor of phenylalanine-tRNA synthetase, which has a greater affinity for OTA than phenylalanine, thus inhibiting the synthesis of intracellular proteins.

Mechanism of action

Ochratoxin is produced by Aspergillus ochraceus and Penicillium viridicatum

A kind of fungal nephrotoxin produced can be divided into two types: A and B. A is more toxic. Ochratoxin Ochratoxin can produce ochratoxin with a toxic concentration at a low temperature of 4°C. Animals ingesting 1ppm body weight dose of ochratoxin A can be lethal within 5-6 days. Common lesions are renal tubular epithelial injury and necrosis of intestinal lymph glands. Feeding a diet containing 1ppm ochratoxin for 3 months can cause polydipsia, frequent urination, growth retardation and reduced feed utilization in animals; feeding diets as low as 200ppb can detect kidney damage for several weeks. Other clinical symptoms include diarrhea, anorexia, and dehydration. Sometimes the clinical symptoms are not obvious, and in areas where ochratoxin poisoning is endemic, the only observable lesions in animals at the time of slaughter are pale and hard kidneys.

Pathological mechanism

?. Ochratoxin A blocks the action of amino acid tRNA synthetase and affects protein synthesis, reducing IgA, IgG and IgM, and reducing antibody titer.

? Damage to poultry Bursa of Fabricius and intestinal lymph tissue of livestock and poultry, reduce the production of antibodies, and affect humoral immunity, which is related to the carcinogenic effect of ochratoxin.

?, cause the phagocytic capacity of granulocytes to decrease, thereby affecting phagocytosis and cellular immunity.

?. Ochratoxin A can affect the development and maturation of fetal tissues and organs through the placenta.

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