Aflatoxin Q1.  Newly identified major metabolite of aflatoxin B1 in monkey liver

Ms, Masri; Wf, Haddon; Re, Lundin; Dp, Hsieh

doi:10.1021/jf60193a050

Cited by 33 publications

(9 citation statements)

References 13 publications

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“…For example, AFM1 was found in most tissues of chickens receiving a diet containing 2,057 ppb AFB1 for 35 days (Chen et al, 1984); the highest level was found in the liver and kidneys, which relates to the important role of these organs in the biotransformation and elimination of xenobiotics, respectively. AFQ1 results from the 3 -hydroxylation of AFB1 and it was first discovered as a major metabolite of AFB1 from monkey liver microsomal incubations (Masri et al, 1974). The predominant enzyme responsible for AFQ1 formation in human liver microsomes is CYP3A4 (Raney et al, 1992b) and AFQ1 is considered to be a major metabolite of AFB1 in humans and monkeys in vitro .…”

Section: Hydroxylation and Hydration Of Aflatoxin B1mentioning

confidence: 99%

Biotransformation of Aflatoxin B1 and Its Relationship with the Differential Toxicological Response to Aflatoxin in Commercial Poultry Species

Díaz¹,

Murcia²

2011

Aflatoxins - Biochemistry and Molecular Biology

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Section: Hydroxylation and Hydration Of Aflatoxin B1mentioning

confidence: 99%

Biotransformation of Aflatoxin B1 and Its Relationship with the Differential Toxicological Response to Aflatoxin in Commercial Poultry Species

Díaz¹,

Murcia²

2011

Aflatoxins - Biochemistry and Molecular Biology

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“…It is hydroxylated at carbon atom ~ to the carbonyl function of the cyclopentenone ring. Aflatoxin O.1 represents one-third to one-half of the metabolites produced from AFB1 by human (Biichi et al, 1974) or monkey liver (Masri et al, 1974b) microsomes but only a small fraction of the AFB1 metabolites produced by chicken or rat liver microsomes (Masri et al, 1974a). Aflatoxin Q1 appears to be much less toxic than AFBt (Hsieh et al, 1974) suggesting its formation to be a mechanism of detoxification in primates.…”

Section: Aflatoxinsmentioning

confidence: 99%

Hepatic Metabolism and Bioactivation of Mycotoxins and Plant Toxins

Swick

1984

Journal of Animal Science

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The intoxication of livestock from ingested feed contaminated with naturally occurring toxicants is of great economic importance. Certain toxicants require enzymatic bioactivation before harmful effects are exhibited. In the liver, the cytochrome P-450 dependent mixed function oxidase (MFO) system normally metabolizes foreign compounds (xenobiotics) into more polar, more excretable and less toxic metabolites. During metabolism of aflatoxins and pyrrolizidine alkaloids (PA), oxidized metabolites are highly reactive with cellular components and are more toxic than the parent compounds. Hepatic bioactivation is of considerable importance because active metabolites are formed directly within the tissues of the animal. In addition, the MFO system has only limited specificity and is dependent on many factors including diet, age, sex, species and environmental influences. The interrelationship of these factors on aflatoxicosis and pyrrolizidine alkaloidosis are often responsible for the chronic nature and difficult etiology of these diseases. A better understanding of the factors affecting metabolism and bioactivation of these toxicants may lead to the development of techniques for protecting animals that are subjected to contaminated feeds.

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“…7), one of the most recently identified aflatoxin metabolites (Biichi et al, 1974;Masri et al, 1974b;Roebuck, 1975); its production from AFB! also appears to require the NADPH monooxygenase system .…”

Section: Aflatoxin Q Xmentioning

confidence: 99%

“…also appears to require the NADPH monooxygenase system . AFQj has not yet been reported as a urinary metabolite, perhaps because little, if any, of the derivative seems to be conjugated (Masri et al, 1974b). Hsieh and co-workers (1974b) estimated that AFQ X was about 18 times less toxic CH, than AFBj to chick embryos and was not mutagenic in a bacterial assay that included rat liver microsomes.…”

Section: Aflatoxin Q Xmentioning

confidence: 99%

Metabolic activation of mycotoxins by animals and humans: An overview

Shank

1977

Journal of Toxicology and Environmental Health

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Aflatoxins are associated with acute toxicoses in poultry and livestock and with liver cancer in human populations in Africa and Southeast Asia. Comparative metabolism studies indicate that aflatoxin B1, the most potent of these compounds, requires metabolic activation to the ultimate carcinogen. The mycotoxin (1) is oxidatively demethylated to form the phenolic derivative, (2) is hydroxylated directly at three sites, and (3) undergoes reduction of the carbonyl group in the cyclopentenone ring to a hydroxyl group; these five hydroxy derivatives all appear to be part of detoxication pathways. Considerable evidence is now available to support the hypothesis that activation of aflatoxin B1 to the ultimate carcinogen involves epoxidation of the double bond in the terminal furan ring. The epoxide decomposes to form a carbonium ion at C-2, which attacks nucleophilic sites in DNA, especially on the guanine moiety. Thus, like carcinogenic polycyclic hydrocarbons and N-nitroso compounds, aflatoxin B1 appears to be activated to an alkylating agent.

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Aflatoxin Q1. Newly identified major metabolite of aflatoxin B1 in monkey liver

Cited by 33 publications

References 13 publications

Biotransformation of Aflatoxin B1 and Its Relationship with the Differential Toxicological Response to Aflatoxin in Commercial Poultry Species

Biotransformation of Aflatoxin B1 and Its Relationship with the Differential Toxicological Response to Aflatoxin in Commercial Poultry Species

Hepatic Metabolism and Bioactivation of Mycotoxins and Plant Toxins

Metabolic activation of mycotoxins by animals and humans: An overview

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