Journal Article

Systemic genotoxic effects produced by light, and synergism with cigarette smoke in the respiratory tract of hairless mice

Roumen M. Balansky, Alberto Izzotti, Francesco D'Agostini, Anna Camoirano, Maria Bagnasco, Ronald A. Lubet and Silvio De Flora

in Carcinogenesis

Volume 24, issue 9, pages 1525-1532
Published in print September 2003 | ISSN: 0143-3334
Published online September 2003 | e-ISSN: 1460-2180 | DOI: http://dx.doi.org/10.1093/carcin/bgg108
Systemic genotoxic effects produced by light, and synergism with cigarette smoke in the respiratory tract of hairless mice

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No information is available on the interaction between cigarette smoke, the most important man-made carcinogen, and light, the most widespread natural carcinogen. In order to clarify this issue, SKH-1 hairless mice were exposed to environmental smoke and/or to the light emitted by sunlight-simulating halogen quartz bulbs. After 28 days, intermediate biomarkers were evaluated in skin, respiratory tract, bone marrow and peripheral blood. The results showed that, individually, the light produced extensive alterations not only in the skin but even at a systemic level, as shown by formation of bulky DNA adducts in both lung and bone marrow and induction of cytogenetic damage in bone marrow and peripheral blood erythrocytes. Smoke damaged the respiratory tract and produced significant alterations in the skin as well as an evident cytogenetic damage in both bone marrow and peripheral blood. Interestingly, as compared with exposure to smoke only, alternate daily cycles of exposure to both light and smoke significantly increased malondialdehyde concentrations and DNA adduct levels in lung and the frequency of micronuclei in pulmonary alveolar macrophages. The oral administration of sulindac, a non-steroidal anti-inflammatory drug, attenuated several biomarker alterations due to the combined exposure of mice to light and smoke. In conclusion, the light induces a systemic genotoxic damage, which is presumably due to the UV-mediated formation in the skin of long-lived derivatives, such as aldehydes. This damage may mechanistically be involved in light-related hematopoietic malignancies. In addition, the light displayed an insofar unsuspected synergism with smoke in the induction of DNA damage in the respiratory tract.

Keywords: COX, cyclooxygenases; CS, cigarette smoke; DRZ, diagonal radioactive zone; ECS, environmental cigarette smoke; LI, labeling index; MDA, malondialdehyde; MN, micronucleated; NCE, normochromatic erythrocytes; 8-OH-dG, 8-hydroxy-2′-deoxyguanosine; PAM, pulmonary alveolar macrophages; PCE, polychromatic erythrocytes; PCNA, proliferating cell nuclear antigen; PN, polynucleated; SBC, sunburn cells; TBA, thiobarbituric acid; TLC, thin-layer chromatography; TUNEL, TdT-mediated dUTP nick end labeling

Journal Article.  6953 words.  Illustrated.

Subjects: Clinical Cytogenetics and Molecular Genetics

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