Archives of Toxicology

, Volume 87, Issue 5, pp 915–918

Oxidative stress in the lung of mice exposed to cigarette smoke either early in life or in adulthood

Authors

  • Rosanna T. Micale
    • Department of Health SciencesUniversity of Genoa
  • Sebastiano La Maestra
    • Department of Health SciencesUniversity of Genoa
  • Angela Di Pietro
    • Department of Hygiene, Public Health and Preventive MedicineUniversity of Messina
  • Giuseppa Visalli
    • Department of Hygiene, Public Health and Preventive MedicineUniversity of Messina
  • Barbara Baluce
    • Department of Hygiene, Public Health and Preventive MedicineUniversity of Messina
    • Cell Factory, Department of Regenerative Medicine, Fondazione IRCCS Ca’ GrandaOspedale Maggiore Policlinico
  • Roumen Balansky
    • Department of Health SciencesUniversity of Genoa
    • National Center of Oncology
  • Vernon E. Steele
    • National Cancer Institute
    • Department of Health SciencesUniversity of Genoa
Short Communication

DOI: 10.1007/s00204-012-0993-1

Cite this article as:
Micale, R.T., Maestra, S.L., Pietro, A.D. et al. Arch Toxicol (2013) 87: 915. doi:10.1007/s00204-012-0993-1

Abstract

Birth and early life stages are critical periods characterized by severe alterations of the redox balance and by “physiological” genomic changes in lung cells, which may be responsible for cancer and other diseases in adulthood. Oxidative stress is a major mechanism accounting for the carcinogenicity of cigarette smoke (CS), which becomes more potently carcinogenic in mice when exposure starts at birth and continues early in life. We compared herewith a variety of end-points related to oxidative stress, mitochondrial alterations, and cell turnover in the lung of Swiss H mice, either sham-exposed or CS-exposed for 4 weeks, starting either at birth or at 4 months of age. The results showed that the physiological levels of certain end-points are affected by age. In fact, the baseline proportion of hypodiploid cells and the mitochondrial potential and mass were higher in adults, whereas 8-hydroxy-2′-deoxyguanosine (8-oxo-dGuo) levels, the proportion of necrotic cells, and the extent of autophagy were higher early in life. Adult mice were more responsive to CS by increasing the proportion of necrotic cells and of cells in S/G2 phase, whereas young mice maintained a high extent of autophagy, exhibited a greater increase of lipid peroxidation products and 8-oxo-dGuo levels, and had a higher frequency of micronucleated cells. In addition, exposure to CS affected the mitochondrial potential/mass, especially in young mice. In conclusion, these data provide evidence that oxidative stress and the resulting DNA damage provide a major contribution to the high susceptibility of mice to CS early in life.

Keywords

Cigarette smokeMouse lungAgeOxidative stressMitochondrial alterations

Supplementary material

204_2012_993_MOESM1_ESM.doc (34 kb)
Supplementary material 1 (DOC 34 kb)

Copyright information

© Springer-Verlag Berlin Heidelberg 2013