Toxicity and carcinogenicity of furan in human diet

@article{Bakhiya2010ToxicityAC,
  title={Toxicity and carcinogenicity of furan in human diet},
  author={Nadiya Bakhiya and Klaus Erich Appel},
  journal={Archives of Toxicology},
  year={2010},
  volume={84},
  pages={563-578}
}
Furan is formed during commercial or domestic thermal treatment of food. The initial surveys of furan concentrations in heat-treated foods, published by European and US authorities, revealed the presence of relatively high furan levels in coffee, sauces, and soups. Importantly, furan is consistently found in commercial ready-to-eat baby foods. Furan induces hepatocellular tumors in rats and mice and bile duct tumors in rats with a high incidence. Epidemiological studies are not available. It is… 

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Low dose assessment of the carcinogenicity of furan in male F344/N Nctr rats in a 2-year gavage study.

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In vivo genotoxicity of furan in F344 rats at cancer bioassay doses.

Lack of genotoxic mechanisms in early‐stage furan‐induced hepatocellular tumorigenesis in gpt delta rats

It is hypothesized that cell proliferation following signal transduction other than the mitogen‐activated protein kinase (MAPK)/ERK pathway may play a crucial role in early‐stage furan‐induced hepatocarcinogenesis.

Subchronic Oral Toxicity Study of Furan in B6C3F1 Mice

A no-observed adverse effect level of 0.12 mg/kg bw per day of furan in mice is suggested to characterize non-neoplastic effects, including those affecting clinical biochemistry, hematology, tissue morphology, and histopathology.

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Proteomic Analysis of Subchronic Furan Exposure in the Liver of Male Fischer F344 Rats

Evaluated toxicoproteomic changes by 2-dimensional differential in gel electrophoresis followed by mass spectrometry analysis revealed that males were more sensitive than females and could lead to adverse health effects at higher doses of furan administration.
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References

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Data requirements for risk assessment of furan in food

There is evidence to indicate that furan-induced carcinogenicity is probably attributable to a genotoxic mechanism, however, chronic toxicity with secondary cell proliferation may indirectly amplify the tumour response.

Assessment of in vivo genotoxicity of the rodent carcinogen furan: evaluation of DNA damage and induction of micronuclei in mouse splenocytes.

Results indicate that the in vivo exposure to furan gives rise to pre-mutagenic DNA damage in resting splenocytes, which remains undetectable until it is converted in frank lesions during the S-phase upon mitogen stimulation.

Impact of various food ingredients on the retention of furan in foods.

Baby food containing spinach showed the highest furan concentration (172 ppb) as well as the highestfuran retention, which means that the highest retention was found in baby foods with added oils.

Disposition of [14C]furan in the male F344 rat.

From the data obtained in this study it is clear that furan is metabolized to reactive species, apparently primarily in liver, and these intermediates react with protein, and the hepatotoxicity resulting from furan exposure may be due to the reaction of furan metabolites with liver macromolecules.

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Data suggest that mechanisms other than direct DNA‐reactivity might explain the profile of oncogene mutations observed in the mouse liver tumors, including selective promotion of different subpopulations of preneoplastic cells and/or mutational events secondary to sustained cell proliferation or inflammation.

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Furan precursors in food: a model study and development of a simple headspace method for determination of furan.

A model system was developed to investigate the origins offuran and two pathways of furan formation have been identified, the oxidation of polyunsaturated fatty acids at elevated temperatures, and the decomposition of ascorbic acid derivatives.

Degraded protein adducts of cis-2-butene-1,4-dial are urinary and hepatocyte metabolites of furan.

Reaction of BDA with N-acetylcysteine or GSH in the presence of lysine indicated that both the alpha- and the epsilon-amino groups ofLysine can be modified by thiol-BDA, suggesting that there are multiple pathways by which furan can modify cellular nucleophiles.

Prediction of furan pharmacokinetics from hepatocyte studies: comparison of bioactivation and hepatic dosimetry in rats, mice, and humans.

One important consequence of blood flow limitation of furan bioactivation is that the amount of toxic metabolite formed in the liver will be unaffected by increases in Vmax due to the induction of cytochrome P450 2E1.
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