DNA damage by mycotoxins.

@article{Wang1999DNADB,
  title={DNA damage by mycotoxins.},
  author={J. S. Wang and John D. Groopman},
  journal={Mutation research},
  year={1999},
  volume={424 1-2},
  pages={
          167-81
        }
}

The Carcinogenicity of Aflatoxin B1

  • J. LiMengxi Liu
  • Biology, Chemistry
    Aflatoxin B1 Occurrence, Detection and Toxicological Effects
  • 2020
This chapter will provide important information on the carcinogenicity of AFB1, including DNA damage checkpoint response and epigenetic alteration, which may potentially be beneficial for the treatment of HCC.

Metabolic Changes of Aflatoxin B1 to become an Active Carcinogen andthe Control of this Toxin

The present review englobes the main characteristics of Aflatoxins as mutagens and carcinogens for humans, their physicochemical properties, the producing fungi, susceptible crops, effects and metabolism.

Antigenotoxic Studies of Different Substances to Reduce the DNA Damage Induced by Aflatoxin B1 and Ochratoxin A

This article reviews the main strategies used to control AFB1 and ochratoxin A and contains an analysis of some antigenotoxic substances that reduce the DNA damage caused by these mycotoxins.

Cellular Responses to Aflatoxin-Associated DNA Adducts

  • M. Fasullo
  • Biology, Chemistry
    DNA Repair- An Update
  • 2019
Aflatoxin B1 (AFB1) is the most potent known hepatocarcinogen and the signature p53 mutation that is found in AFB1-associated liver cancer suggests that AFB1 is a potent genotoxin, and pathways function to detoxify the metabolically active intermediate, excise resulting DNA adducts, bypass unrepairedAdducts and repair secondary DNA breaks.

Research progress in toxicological effects and mechanism of aflatoxin B1 toxin

Fungal contamination of animal feed can severely affect the health of farm animals, and result in considerable economic losses. Certain filamentous fungi or molds produce toxic secondary metabolites

Antineoplastic potential of mycotoxins.

This work has concluded that highly cytotoxic mycotoxins with tolerable side effects, combined with an antineoplastic character, could be potential candidates against metastasis.

DNA damage in human fibroblasts exposed to fumonisin B(1).

Research Section DNA damage in human fibroblasts exposed to fumonisin B1

The results indicate that DNA damage of apoptotic type in human fibroblasts is caused by exposure to FB1 at high concentrations and for a prolonged time and that the genotoxic potential of FB1 has probably been underestimated and should be reconsidered.
...

References

SHOWING 1-10 OF 95 REFERENCES

Cellular interactions and metabolism of aflatoxin: an update.

Genotoxicity of zearalenone, an estrogenic mycotoxin: DNA adduct formation in female mouse tissues.

The results confirm the genotoxicity of zearalenone and its ability to induce hepatocellular adenomas, rather than tumours of genital organs, in mice.

Mutational properties of the primary aflatoxin B1-DNA adduct.

It is concluded that the AFB1-N7-Gua adduct, and not the apurinic site, has genetic requirements for mutagenesis that best explain mutations in aflatoxin-treated cells.

Quantitative comparison of covalent aflatoxin-DNA adducts formed in rat and mouse livers and kidneys.

In vitro studies on the activation of AFB1 by microsomal fractions of mouse and rat livers found that mouse liver microsomes were rapidly inactivated, and a good correlation was found between the level of covalent modification of DNA, species sensitivity, and organ specificity, to the toxic effects of AFB 1.

Quantitative Comparison of Formed in Rat and Mouse Covalent Aflatoxin-DNA Livers and Kidneys

In vitro studies on the activation of AFB1 by microsomal fractions of mouse and rat livers found that mouse liver microsomes were rapidly inactivated, and a good correlation was found between the level of covalent modification of DNA, species sensitivity, and organ specificity, to the toxic effects of AFB 1.

DNA adduct formation in mice treated with ochratoxin A.

The genotoxicity of ochratoxin A is confirmed using a modified 32P-postlabelling method, the sensitivity of which was improved by treatment with nuclease P1, and DNA isolated from liver, kidney and spleen was found.

Structural identification of the major DNA adduct formed by aflatoxin B1 in vitro.

Analysis of spectral and chemical data indicates that the major product of the interaction of metabolically activated aflatoxin B1 and DNA is 2,3-dihydro-2-(N7-guanyl)-3-hydroxyaflatoxin B 1 with the guanine and hydroxyl functions possessing a trans configuration.

Molecular dosimetry of urinary aflatoxin-N7-guanine and serum aflatoxin-albumin adducts predicts chemoprotection by 1,2-dithiole-3-thione in rats.

Levels of molecular dosimetry biomarkers for determining genotoxic damage caused by aflatoxin B1 have been measured in a chronic exposure model with male F344 rats and suggest that these biomarkers are predictive short-term, non-invasive measures for assessing the efficacy of chemoprotective interventions in experimental studies and can be applied to human clinical trials directed at populations at high risk for aflat toxin exposure and primary hepatocellular carcinoma.

Potent inhibition of aflatoxin-induced hepatic tumorigenesis by the monofunctional enzyme inducer 1,2-dithiole-3-thione.

A broad pattern of induction of detoxication enzymes by 1,2-dithiole-3-thione supports the potential widespread use of this compound as a protective agent against chemical carcinogenesis and other forms of electrophile toxicity.
...