Serum antioxidant capacity and oxidative injury to pulmonary DNA in never-smokers with primary lung cancer

Kensaku Ito, Tokujiro Yano, Yosuke Morodomi, Tsukihisa Yoshida, Mikihiro Kohno, Akira Haro, Yasunori Shikada, Tatsuro Okamoto, Riichiroh Maruyama, Yoshihiko Maehara

Research output: Contribution to journalArticlepeer-review

17 Citations (Scopus)

Abstract

Background/Aim: Recently, in spite of the decrease in smoking in developed nations, the prevalence of primary lung cancer has been increasing in never-smokers. In the present study, we examined the status of oxidative stress and attempted to clarify the influence of oxidative stress in non-smoking patients with lung cancer. Patients and Methods: Sixty-one lung cancer patients who underwent a surgical resection, including 27 never-smokers and 34 ever-smokers with a history of more than 20 pack-years, were included. In addition, 18 surgical patients with benign lung diseases treated during the same period were also included as non-malignant controls. Using blood samples, both serum oxidative stress (OS) and anti-oxidant capacity (AOC) were examined with the derivatives of reactive oxygen metabolites (D-Roms) test and the biological antioxidant power (BAP) test, respectively. To assess the oxidative damage of the DNA in lung tissues, the non-lesion site tissues of the lung were immunohistochemically examined for the accumulation of thymidine glycol (TG). Results: There was no significant relationship between the serum OS level and various clinicopathological factors including the patient age, sex, body mass index, pathologic stage, and smoking status. On the other hand, the mean level of AOC was significantly lower in never-smokers than in ever-smokers. Although the mean TG-positive rate in ever-smokers was significantly higher than that in never-smokers, the mean TG-positive rate of the latter was significantly higher than that of patients with benign diseases. Conclusion: The present study first demonstrated the low AOC in never-smokers with NSCLC, which may be a factor contributing to excessive oxidative DNA damage in the lung tissues.

Original languageEnglish
Pages (from-to)1063-1067
Number of pages5
JournalAnticancer research
Volume32
Issue number3
Publication statusPublished - Mar 2012

All Science Journal Classification (ASJC) codes

  • Oncology
  • Cancer Research

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