Identification of early target genes of aflatoxin B1 in human hepatocytes, inter-individual variability and comparison with other genotoxic compounds

Jossé, Rozenn; Dumont, Julie; Fautrel, Alain; Robin, Marie-Anne; Guillouzo, André

doi:10.1016/j.taap.2011.10.019

Cited by 53 publications

(35 citation statements)

References 47 publications

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“…There is an association between carcinogenicity of AFB1 and the alteration of several p53-target gene expressions and mutations, mainly the p53 codon 249 hotspot mutations (Josse et al, 2012). Several reports have shown the detrimental effects of AFB1 on the liver (Hassan et al, 2015), testis, epididymis (Agnes and Akbarsha, 2001;Hamzawy et al, 2012), Kidney (Abdel-Hamid and Firgany Ael, 2015;Arora et al, 1978), Heart (Abdulmajeed, 2011;Mohamed and Metwally, 2009), ovary (Ibeh et al, 2000), and the brain (Bahey et al, 2015).…”

Section: Issn: 2319-7706 Volume 7 Number 04 (2018)mentioning

confidence: 99%

Assessment of Genotoxic and Cytogenetic Effects of Aflatoxin B1 in Mouse Bone Marrow Cells

Algarni¹

2018

Int.J.Curr.Microbiol.App.Sci

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Section: Issn: 2319-7706 Volume 7 Number 04 (2018)mentioning

confidence: 99%

Assessment of Genotoxic and Cytogenetic Effects of Aflatoxin B1 in Mouse Bone Marrow Cells

Algarni¹

2018

Int.J.Curr.Microbiol.App.Sci

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“…Metabolizing AFB1 increases the production of free radicals and lipid peroxides, resulting in cell damage [43,44]. AFB1 is activated in the liver by CYP450 to AFB1-8,9-epoxide, which forms adducts with both DNA and protein.…”

Section: Efects On Oxidative Stress Of Alatoxinmentioning

confidence: 99%

The Effect on Oxidative Stress of Aflatoxin and Protective Effect of Lycopene on Aflatoxin Damage

Yılmaz¹,

Kaya²,

Kisaçam³

2017

Aflatoxin-Control, Analysis, Detection and Health Risks

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Alatoxin (AF) is polysubstituted bifuranocoumarins that are secondary fungal metabolites produced by parasiticus/lavus group of the genus Aspergillus. AF is hepatotoxic, nephrotoxic, mutagenic, teratogenic, genotoxic, and immunotoxic, so the International Agency for Research on Cancer has classiied AF as class I human carcinogen. AF-mediated cell injury may be associated with the release of free radicals, and these radicals initiate lipid peroxidation and a damaging process in biological systems since all cell membranes contain the polyunsaturated faty acids (PUFAs), which are substrates for such a reaction. One of the causes for AF-induced toxicity is the oxidative stress, which leads to the improved generation of reactive oxygen species (ROS) and the oxidative DNA damage. Lycopene, a naturally occurring carotenoid, has drawn a particular atention in recent years because of its high antioxidant activity and free radical scavenging capacity and has been shown to be efective against oxidative stress due to AF. Lycopene blocks Phase 1 metabolic enzymes of AFB such as 3A4, 2A6, and 1A2.

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“…25,26 In human hepatocytes in vitro Josse and colleagues found that FHIT was an early target gene following exposure to the genotoxic carcinogen aflatoxin B1. 27 In the rat, Fhit is located on chromosome 15 and many studies suggest that its lost is an early event in carcinogenesis. [28][29][30][31] Although we saw a decrease in expression of Fhit gene in both kidney and the liver, the decrease was only statistically significant in the liver at the protein level (Fig.…”

Section: In Vivo Studiesmentioning

confidence: 99%

Transcriptomic alterations induced by Monuron in rat and human renal proximal tubule cells in vitro and comparison to rat renal-cortex in vivo

et al. 2015

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-dimethyl-3-(4-chlorophenyl)urea) is a non-selective phenylurea herbicide, widely used in developing countries although concerns have been raised about its toxicity and carcinogenicity. Monuron was evaluated by the National Toxicology Program in 1988 and shown to be a male rat-specific renal carcinogen. We report that oral administration of Monuron to male rats for 3 days, leads to a larger number of genes being differentially expressed in the renal-cortex than in the liver. Further, we observed up-regulation of cell cycle genes and genes involved in cell proliferation in the renalcortex while in the liver xenobiotic metabolising enzymes were up-regulated. We also identified one commonly down-regulated gene in both organs -fragile histidine triad gene (Fhit), a putative tumour suppressor gene; however the down-regulation was only significant at the protein level in the liver. In addition, we conducted in vitro wholegenome transcriptomics studies with human and rat renal cortical cells. Rat cells exposed to Monuron showed down-regulation of sterol biosynthesis, spliceosome and cell cycle genes and up-regulation of genes involved in amino acid metabolism and transport. No genes were found to be differentially expressed in human cells exposed to Monuron. Overall, the findings from the in vitro studies showed very little overlap with the whole animal findings.

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Identification of early target genes of aflatoxin B1 in human hepatocytes, inter-individual variability and comparison with other genotoxic compounds

Cited by 53 publications

References 47 publications

Assessment of Genotoxic and Cytogenetic Effects of Aflatoxin B1 in Mouse Bone Marrow Cells

Assessment of Genotoxic and Cytogenetic Effects of Aflatoxin B1 in Mouse Bone Marrow Cells

The Effect on Oxidative Stress of Aflatoxin and Protective Effect of Lycopene on Aflatoxin Damage

Transcriptomic alterations induced by Monuron in rat and human renal proximal tubule cells in vitro and comparison to rat renal-cortex in vivo

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