High susceptibility of neonatal mice to molecular, biochemical and cytogenetic alterations induced by environmental cigarette smoke and light

Flora, Silvio De; D’Agostini, Francesco; Balansky, Roumen; Camoirano, Anna; Cartiglia, Cristina; Longobardi, M.; Travaini, Giorgia; Steele, Vernon E.; Pesce, Carlo; Izzotti, Alberto

doi:10.1016/j.mrrev.2007.11.004

Cited by 28 publications

(41 citation statements)

References 36 publications

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“…These findings support the conclusions of our previous studies showing the ability of ECS to induce genotoxic damage and other alterations of intermediate biomarkers in various cells, tissues, and organs of rodents exposed in vivo (5,10,21,22,(40)(41)(42)(43)(44)(45)(46)(47)(48)(49)(50)(51)(52).…”

Section: Discussionsupporting

confidence: 92%

“…Cancer Prevention Research their dams to ECS-induced alterations of early biomarkers (21,22). Budesonide and PEITC are among the most promising chemopreventive agents.…”

Section: Discussionmentioning

confidence: 99%

“…8-oxodGuo levels were quantified by calculating the ratio between cpm detected in the 8-oxodGuo-related spot and cpm detected in normal nucleotides and expressed as 8-oxodGuo/10 5 nucleotides. A DNA-free sample was used as a negative control, and four reference standards were used for 8-oxodGuo identification, as previously detailed (21).…”

Section: Evaluation Of Intermediate Biomarkersmentioning

confidence: 99%

“…Thereafter, preliminarily to the chemoprevention study reported in the present study, we did a carcinogenicity study in CD-1 albino mice exposed to ECS since birth for a period of 4 months. After weanling, subgroups of sham-exposed mice and of ECS-exposed mice were sacrificed and evaluated for a variety of intermediate biomarkers in the respiratory tract and hematopoietic system (21) and in the cardiocirculatory system (22). Many biomarkers were significantly increased in ECS-exposed mice, including levels of bulky DNA adducts and oxidatively generated DNA damage in lung, heart, and aorta, amounts of thiobarbituric acid reactive substances in lung, loss of Fhit protein and apoptosis in pulmonary alveolar macrophages and bronchial epithelial cells, proliferation of bronchial epithelial cells, and cytogenetical damage in bone marrow and peripheral blood erythrocytes.…”

mentioning

confidence: 99%

“…Many biomarkers were significantly increased in ECS-exposed mice, including levels of bulky DNA adducts and oxidatively generated DNA damage in lung, heart, and aorta, amounts of thiobarbituric acid reactive substances in lung, loss of Fhit protein and apoptosis in pulmonary alveolar macrophages and bronchial epithelial cells, proliferation of bronchial epithelial cells, and cytogenetical damage in bone marrow and peripheral blood erythrocytes. Interestingly, the response to ECS, in terms of several biomarkers, was more pronounced in post-weanling females than in their dams, kept in the same cages (21,22). Eleven months after birth and 7 months after stopping exposure to ECS, all surviving mice were sacrificed.…”

mentioning

confidence: 99%

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Modulation by Phenethyl Isothiocyanate and Budesonide of Molecular and Histopathologic Alterations Induced by Environmental Cigarette Smoke in Mice

D’Agostini

Mastracci

Izzotti

et al. 2009

Cancer Prevention Research

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Our discovery that the perinatal period involves nucleotide modifications and gene overexpression in mouse lung prompted us to evaluate whether mice may become more susceptible to cigarette smoke when exposure starts immediately after birth. We previously showed that mainstream cigarette smoke is a quite potent carcinogen in neonatal mice. Further on, we showed that exposure of mice to environmental cigarette smoke (ECS), starting at birth, results in alterations of a variety of intermediate biomarkers. However, after 4 months of exposure to ECS followed by 7 months of recovery in filtered air, the lung tumor yield was rather low. In the present study, we evaluated the protective effects of the glucocorticoid budesonide and of the dietary agent phenethyl isothiocyanate in mice exposed to ECS for 9 months followed by 2 months of recovery. After weanling, the mice exposed to ECS since birth underwent a variety of alterations of molecular and cytogenetical end points, and 11 months after birth, they exhibited significant histopathologic changes, such as pulmonary anthracosis, emphysema, hemorrhagic areas, alveolar bronchiolarization, bronchial hyperplasia, and tumors, both benign and malignant. The carcinogenic response was less evident in dams exposed to ECS under identical conditions. Both phenethyl isothiocyanate and budesonide, administered daily with the diet after weanling, attenuated several alterations of ECS-related biomarkers and moderately protected the lungs from histopathologic alterations, including tumors. Thus, although not as efficiently as the bioassay in mainstream cigarette smoke-exposed mice, the model in neonatal mice is suitable to evaluate both ECS carcinogenicity and its modulation by chemopreventive agents.

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Section: Discussionsupporting

confidence: 92%

“…Cancer Prevention Research their dams to ECS-induced alterations of early biomarkers (21,22). Budesonide and PEITC are among the most promising chemopreventive agents.…”

Section: Discussionmentioning

confidence: 99%

Section: Evaluation Of Intermediate Biomarkersmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Modulation by Phenethyl Isothiocyanate and Budesonide of Molecular and Histopathologic Alterations Induced by Environmental Cigarette Smoke in Mice

D’Agostini

Mastracci

Izzotti

et al. 2009

Cancer Prevention Research

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Impact of oncology‐related direct‐to‐consumer advertising

Abel

Chen

Taback

et al. 2012

Cancer

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BACKGROUND:Little is known about the impact of direct-to-consumer advertising (DTCA) on appropriate versus inappropriate prescribing. Aromatase inhibitor (AI) therapy for breast cancer provides an ideal paradigm for studying this issue, because AIs have been the focus of substantial DTCA, and because they should only be used in postmenopausal women, age can serve as a simple surrogate marker of appropriateness. METHODS: Data regarding national DTCA spending for the AIs were obtained from TNS Multimedia; hormonal therapy prescription data were obtained from IMS Health. Time series analyses were performed to characterize the association between monthly changes in DTCA spending for the AIs and monthly changes in the proportion of all new hormonal therapy prescriptions represented by the AIs from October 2005 to September 2007. Analyses were stratified by age, considering prescriptions for women 40 (likely premenopausal) to be inappropriate and those for women > 60 (likely postmenopausal) to be appropriate. RESULTS: Monthly dollars spent on AI-associated DTCA varied considerably ($118,600 to $22,019,660). Time series analysis revealed that for every million dollars spent on DTCA for the AIs, there was an associated increase 3 months later in the new AI prescription proportion of 0.15% for all ages (P < .0001) and 0.18% for those > 60 years (P < .0001), but no significant change for those 40 at any time from 0 to 6 months. CONCLUSIONS: DTCA for the AIs was associated with increases in appropriate prescriptions with no significant effect on inappropriate prescriptions, suggesting that DTCA may not foster inappropriate medication use for certain drug classes. Cancer 2013;119:1065-72.

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Preneoplastic and neoplastic lesions in the lung, liver and urinary tract of mice exposed to environmental cigarette smoke and UV light since birth

D’Agostini

Balansky

Steele

et al. 2008

Intl Journal of Cancer

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It is difficult to reproduce the carcinogenicity of cigarette smoke (CS) in animal models. Recently, we showed that exposure of mice to mainstream CS (MCS) for 120 days, starting immediately after birth, resulted in an early and potent carcinogenic response. In parallel, we implemented studies evaluating intermediate biomarkers and tumors in mice exposed to environmental CS (ECS). To this purpose, we used 263 newborn CD-1 mice born from 27 dams. The whole-body exposure to ECS for 120 days, starting within 12 hr after birth, resulted in an early appearance of preneoplastic lesions in lung, which however tended to attenuate after discontinuing exposure. When the experiment was stopped, after 330 days, the number of lung adenomas was higher in ECSexposed mice as compared to sham-exposed mice, but such increase was statistically significant only in mice co-exposed to smoke and halogen light mimicking solar irradiation. Moreover, exposure to ECS produced extensive histopathological changes, mainly parenchymatous degeneration, in liver. The alterations produced in both lung and liver require that exposure to ECS starts immediately after birth, no effect being observed when exposure started 8 days later. In contrast, induction by ECS of alterations in the urinary tract, such as microadenomas and adenomas in renal pelvis and kidney, papillary hyperplasia of urothelium, and urinary bladder papillomas, were unrelated to the exposure time after birth. The results obtained with ECS cannot be directly compared to those previously obtained with MCS, since the latter involved shorter daily exposures to more massive CS doses.

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High susceptibility of neonatal mice to molecular, biochemical and cytogenetic alterations induced by environmental cigarette smoke and light

Cited by 28 publications

References 36 publications

Modulation by Phenethyl Isothiocyanate and Budesonide of Molecular and Histopathologic Alterations Induced by Environmental Cigarette Smoke in Mice

Modulation by Phenethyl Isothiocyanate and Budesonide of Molecular and Histopathologic Alterations Induced by Environmental Cigarette Smoke in Mice

Impact of oncology‐related direct‐to‐consumer advertising

Preneoplastic and neoplastic lesions in the lung, liver and urinary tract of mice exposed to environmental cigarette smoke and UV light since birth

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