Formation of adducts by bisphenol A, an endocrine disruptor, in DNA in vitro and in liver and mammary tissue of mice

Izzotti, Alberto; Kanitz, S; D’Agostini, Francesco; Camoirano, Anna; Flora, Silvio De

doi:10.1016/j.mrgentox.2009.07.011

Cited by 105 publications

(56 citation statements)

References 48 publications

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“…Our study was the first to suggest the association between hypoalbuminemia and the mortality of IPFD. Albumin has essential physiologic effects necessary for health such as vasodilatation, inhibition of endothelial cell apoptosis, antioxidant effects, reduced platelet aggregation, and marker of inflammation in acute phase response [42][43][44]. Hypoalbuminemia may acts via effects on antibiotics [45], malnutrition after surgery, or the underlying cause of hypoalbuminemia reduces survival.…”

Section: Discussionmentioning

confidence: 99%

Pulmonary Fungal Diseases in Immunocompetent Hosts: A Single-Center Retrospective Analysis of 35 Subjects

et al. 2016

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Section: Discussionmentioning

confidence: 99%

Pulmonary Fungal Diseases in Immunocompetent Hosts: A Single-Center Retrospective Analysis of 35 Subjects

et al. 2016

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“…In contrast, BPA induced numerical chromosomal aberrations and morphological changes in cultured SHE cells (22) and in mice it induced achromatic lesions and c-mitotic effects in bone marrow cells (24). In addition, BPA metabolite(s) were shown to bind to DNA in a cellular system (25)(26), in cultured SHE cells (22), and in rodent liver in vivo (27)(28). Moreover, in oestrogen receptor (ER)-positive MCF-7 cells, BPA caused DNA strand breaks that were ER-dependent (29).…”

mentioning

confidence: 99%

Mutagenicity and DNA Damage of Bisphenol a and its Structural Analogues in Hepg2 Cells

Fic

Žegura

Dolenc

et al. 2013

Archives of Industrial Hygiene and Toxicology

100

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Environmental oestrogen bisphenol A (BPA) and its analogues are widespread in our living environment. Because their production and use are increasing, exposure of humans to bisphenols is becoming a signifi cant issue. We evaluated the mutagenic and genotoxic potential of eight BPA structural analogues (BPF, BPAF, BPZ, BPS, DMBPA, DMBPS, BP-1, and BP-2) using the Ames and comet assay, respectively. None of the tested bisphenols showed a mutagenic effect in Salmonella typhimurium strains TA98 and TA100 in either the presence or absence of external S9-mediated metabolic activation (Aroclor 1254-induced male rat liver). Potential genotoxicity of bisphenols was determined in the human hepatoma cell line (HepG2) at non-cytotoxic concentrations (0.1 μmol L -1 to 10 μmol L -1 ) after 4-hour and 24-hour exposure. In the comet assay, BPA and its analogue BPS induced signifi cant DNA damage only after the 24-hour exposure, while analogues DMBPS, BP-1, and BP-2 induced a transient increase in DNA strand breaks observed only after the 4-hour exposure. BPF, BPAF, BPZ, and DMBPA did not induce DNA damage.

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“…In examination of epigenetic changes in breast epithelial cells treated with low-dose BPA and the effect of BPA on the ER-α signalling pathway and global gene expression profiles, 170 genes with similar expression changes in response to BPA were identified, and the gene suppression by BPA was mediated in part through an ER-α dependent pathway [134]. Administration of BPA to mice confirmed that DNA adducts are formed in target mammary cells (4.7-fold higher than in controls) [135]. Although DNA adducts do not necessarily evolve into tumours or other chronic degenerative diseases, the formation of these molecular lesions in target mammary cells may bear relevance for the potential involvement of BPA in breast carcinogenesis.…”

Section: Bisphenol Amentioning

confidence: 84%

Impact of Environmental Contaminants on Breast Cancer / Wpływ Zanieczyszczenia Środowiska Na Raka Piersi

Kráľová

Jampílek

2015

Ecological Chemistry and Engineering S

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Breast cancer is the most frequent cancer in women. It is believed that among the causes of breast cancer, hereditary factors account for only 5-10% of risk and the environmental exposures to environmental contaminants account for an additional 30-50% of risk. This paper summarizes findings related to the risk of breast cancer due to exposure to following environmental contaminants: polycyclic aromatic hydrocarbons, polychlorinated biphenyls and dioxins, organochlorine pesticides, organophosphorous pesticides, bisphenol A, phthalates, parabens, organic solvents, atmospheric pollutants, alkylphenols, metals, ionizing radiation, electromagnetic field and light pollution. Results obtained in in vitro experiments with breast cancer cell lines and in vivo with model rodents as well as in population based case-control studies are presented and the mode of action of individual environmental contaminants on mammary gland is discussed. Attention is also devoted to the effects of the timing of exposure to environmental contaminants (mainly exposition during development of the mammary gland) on breast cancer risk. Outcomes of professional exposure to some environmental contaminants on breast cancer risk are analysed as well.

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Formation of adducts by bisphenol A, an endocrine disruptor, in DNA in vitro and in liver and mammary tissue of mice

Cited by 105 publications

References 48 publications

Pulmonary Fungal Diseases in Immunocompetent Hosts: A Single-Center Retrospective Analysis of 35 Subjects

Pulmonary Fungal Diseases in Immunocompetent Hosts: A Single-Center Retrospective Analysis of 35 Subjects

Mutagenicity and DNA Damage of Bisphenol a and its Structural Analogues in Hepg2 Cells

Impact of Environmental Contaminants on Breast Cancer / Wpływ Zanieczyszczenia Środowiska Na Raka Piersi

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