Evaluation of the Modifying Effect of Inhalation of Mainstream Cigarette Smoke on Mouse Bladder Carcinogenesis

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Author(s)

    • Kato Minoru Kato Minoru
    • Department of Pathology, Osaka City University Graduate School of Medicine, 1-4-3 Asahimachi, Abeno-ku, Osaka City, Osaka 545-0051, Japan
    • Wei Min Wei Min
    • Department of Pathology, Osaka City University Graduate School of Medicine, 1-4-3 Asahimachi, Abeno-ku, Osaka City, Osaka 545-0051, Japan
    • Fujioka Masaki
    • Department of Pathology, Osaka City University Graduate School of Medicine, 1-4-3 Asahimachi, Abeno-ku, Osaka City, Osaka 545-0051, Japan
    • Kakehashi Anna
    • Department of Pathology, Osaka City University Graduate School of Medicine, 1-4-3 Asahimachi, Abeno-ku, Osaka City, Osaka 545-0051, Japan
    • Wanibuchi Hideki
    • Department of Pathology, Osaka City University Graduate School of Medicine, 1-4-3 Asahimachi, Abeno-ku, Osaka City, Osaka 545-0051, Japan

Abstract

Cigarette smoking is one of the major risk factors of bladder cancer in humans. To date, however, there is no experimental evidence for the effects of inhalation exposure to mainstream cigarette smoke on bladder carcinogenesis. The purpose of the present study was to evaluate the effect of inhalation of mainstream cigarette smoke on mouse bladder carcinogenesis using a cigarette smoke inhalation exposure system. Six-week-old male C57BL mice were administered 0.025% N-butyl-N-(4-hydroxybutyl) nitrosamine (BBN) in their drinking water for 8 weeks and then divided into 2 groups and exposed to 0 or 300 mg/m<sup>3</sup> wet total particulate matter mainstream cigarette smoke for 2 h per day, five times per week, for 22 weeks. The incidences of bladder tumors (papilloma and urothelial carcinoma) tended to increase in the cigarette smoke-exposed group (25.0%) compared with the controls (15.8%), albeit without a statistically significant difference. We also evaluated mRNA expression levels of cytochrome P450 (cyp) enzymes and proliferating cell nuclear antigen (PCNA) in the bladder epithelium. Expression of cyp1a1 was significantly increased in the cigarette smoke-exposed group. Cigarette smoke exposure did not have a significant effect on the expression of cyp1a2, cyp 1b1, cyp 2a4, cyp 2b10, cyp 2e1, or PCNA. In conclusion, limited exposure to mainstream cigarette smoke for 22 weeks, caused a significant increase in cyp1a1 expression. This increase coupled with the nonsignificant increase in bladder tumors suggests that a longer period of exposure is required to clarify the effects of cigarette smoke on bladder carcinogenesis.

Journal

  • Journal of Toxicologic Pathology

    Journal of Toxicologic Pathology 26(4), 447-451, 2013

    JAPANESE SOCIETY OF TOXICOLOGIC PATHOLOGY

Codes

  • NII Article ID (NAID)
    130003382468
  • NII NACSIS-CAT ID (NCID)
    AN10232280
  • Text Lang
    ENG
  • ISSN
    0914-9198
  • NDL Article ID
    025161753
  • NDL Call No.
    Z19-2431
  • Data Source
    NDL  J-STAGE 
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