Aflatoxin B1 metabolism (WP3247)

Bos taurus

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'''Aflatoxins''' are naturally occurring [[wikipedia:mycotoxin|mycotoxin]]s that are produced by many species of ''[[wikipedia:Aspergillus|Aspergillus]]'', a [[wikipedia:fungus|fungus]], most notably ''[[wikipedia:Aspergillus flavus|Aspergillus flavus]]'' and ''[[wikipedia:Aspergillus parasiticus|Aspergillus parasiticus]]''. After entering the body, aflatoxins are metabolized by the liver to a reactive intermediate, aflatoxin M1, an [[wikipedia:epoxide|epoxide]]. Aflatoxin B1 is considered the most toxic and is produced by both Aspergillus flavus and Aspergillus parasiticus. Source: [[wikipedia:Aflatoxin|Wikipedia]]

Authors

Martina Summer-Kutmon

Activity

last edited

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Organisms

Bos taurus

Communities

Annotations

Pathway Ontology

aflatoxin metabolic pathway cellular detoxification pathway

Participants

Label Type Compact URI Comment
Aflatoxin B1 exo-8,9-epoxide-GSH Metabolite pubchem.compound:5460816
aflatoxin B1 Metabolite hmdb:HMDB0006552
Aflatoxin B1 exo-8,9-epoxide Metabolite hmdb:HMDB0006558
Aflatoxin M1 Metabolite pubchem.compound:15558498
Aflatoxin Q1 Metabolite pubchem.compound:104757
AKR7A2 GeneProduct ensembl:ENSBTAG00000026758 HomologyConvert: Homo sapiens to Bos taurus: Original ID = En:ENSG00000053371
CYP1A2 GeneProduct ensembl:ENSBTAG00000000085 HomologyConvert: Homo sapiens to Bos taurus: Original ID = En:ENSG00000140505
AKR7A2 GeneProduct ensembl:ENSBTAG00000012289 HomologyConvert: Homo sapiens to Bos taurus: Original ID = En:ENSG00000162482
CYP2A13 GeneProduct ensembl:ENSBTAG00000047815 HomologyConvert: Homo sapiens to Bos taurus: Original ID = En:ENSG00000197838
EPHX1 GeneProduct ensembl:ENSBTAG00000000140 HomologyConvert: Homo sapiens to Bos taurus: Original ID = En:ENSG00000143819
CYP3A4 GeneProduct ensembl:ENSBTAG00000047379 HomologyConvert: Homo sapiens to Bos taurus: Original ID = En:ENSG00000160868

References

  1. Glutathione S-transferase-catalyzed conjugation of bioactivated aflatoxin B(1) in human lung: differential cellular distribution and lack of significance of the GSTM1 genetic polymorphism. Stewart RK, Smith GB, Donnelly PJ, Reid KR, Petsikas D, Conlan AA, et al. Carcinogenesis. 1999 Oct;20(10):1971–7. PubMed Europe PMC Scholia
  2. Reduction of aflatoxin B1 dialdehyde by rat and human aldo-keto reductases. Guengerich FP, Cai H, McMahon M, Hayes JD, Sutter TR, Groopman JD, et al. Chem Res Toxicol. 2001 Jun;14(6):727–37. PubMed Europe PMC Scholia
  3. Role of genetic polymorphism of glutathione-S-transferase T1 and microsomal epoxide hydrolase in aflatoxin-associated hepatocellular carcinoma. Tiemersma EW, Omer RE, Bunschoten A, van’t Veer P, Kok FJ, Idris MO, et al. Cancer Epidemiol Biomarkers Prev. 2001 Jul;10(7):785–91. PubMed Europe PMC Scholia
  4. Reaction of aflatoxin B(1) oxidation products with lysine. Guengerich FP, Arneson KO, Williams KM, Deng Z, Harris TM. Chem Res Toxicol. 2002 Jun;15(6):780–92. PubMed Europe PMC Scholia
  5. Translational strategies for cancer prevention in liver. Kensler TW, Qian GS, Chen JG, Groopman JD. Nat Rev Cancer. 2003 May;3(5):321–9. PubMed Europe PMC Scholia
  6. Efficient activation of aflatoxin B1 by cytochrome P450 2A13, an enzyme predominantly expressed in human respiratory tract. He XY, Tang L, Wang SL, Cai QS, Wang JS, Hong JY. Int J Cancer. 2006 Jun 1;118(11):2665–71. PubMed Europe PMC Scholia
  7. Cytochrome P450s and other enzymes in drug metabolism and toxicity. Guengerich FP. AAPS J. 2006 Mar 10;8(1):E101-11. PubMed Europe PMC Scholia
  8. CYP2A13 in human respiratory tissues and lung cancers: an immunohistochemical study with a new peptide-specific antibody. Zhu LR, Thomas PE, Lu G, Reuhl KR, Yang GY, Wang LD, et al. Drug Metab Dispos. 2006 Oct;34(10):1672–6. PubMed Europe PMC Scholia
  9. Aldo-keto reductases and bioactivation/detoxication. Jin Y, Penning TM. Annu Rev Pharmacol Toxicol. 2007;47:263–92. PubMed Europe PMC Scholia
  10. The aldo-keto reductase superfamily and its role in drug metabolism and detoxification. Barski OA, Tipparaju SM, Bhatnagar A. Drug Metab Rev. 2008;40(4):553–624. PubMed Europe PMC Scholia