Lack of promotion of 7,12-dimethylbenz[a]anthracene-initiated mouse skin carcinogenesis by 1.5 GHz electromagnetic near fields.

نویسندگان

  • K Imaida
  • K Kuzutani
  • J Wang
  • O Fujiwara
  • T Ogiso
  • K Kato
  • T Shirai
چکیده

The effects of 1.5 GHz electromagnetic near fields of time division multiple access (TDMA) signal for the Personal Digital Cellular, Japanese cellular telephone standard (PDC) used for cellular phones, on mouse skin carcinogenesis initiated by 7,12-dimethylbenz[a]anthracene (DMBA) were examined. Ten-week-old ICR female mice were treated with a single application of DMBA on shaved dorsal skin by painting at a concentration of 100 microg/100 microl acetone per mouse. One week later, mice were divided into four groups, receiving electromagnetic near fields exposure (DMBA-EMF), sham-exposure (DMBA-Sham), 12-O-tetradecanoylphorbol-13-acetate (TPA, 4 microg /200 microl acetone/mouse), as a positive control (DMBA-TPA), and no-treatment (DMBA-Control). EMF near fields exposure conditions were as follows: skin local peak specific absorption rate (SAR) 2.0 W/kg, whole body average SAR 0.084 W/kg (ratio of peak to average SAR is 24), 90 min a day, 5 days a week, for 19 weeks. At week 20, animals were killed and skin tumors were analyzed histopathologically. The incidences of skin tumors in DMBA-EMF, DMBA-Sham, DMBA-TPA and DMBA-Control groups were 0/48 (0%), 0/48 (0%), 29/30 (96.6%) and 1/30 (3.3%), respectively. Histopathologically, papilloma and squamous cell carcinoma (SCC) were observed in the DMBA-TPA group and only papilloma observed in the DMBA-Control group. The incidences of squamous cell papillomas and squamous cell carcinomas in DMBA-TPA and DMBA-Control groups were 29/30 (96.6%) and 1/30 (3.3%), respectively, numbers of tumors per mouse (tumor multiplicity) being 18.8 +/- 13.4 and 0.1 +/- 0.5. These data clearly demonstrated that near fields exposure to 1.5 GHz EMF, used for cellular phones, does not exert any enhancing effect on skin tumorigenesis initiated by DMBA.

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عنوان ژورنال:
  • Carcinogenesis

دوره 22 11  شماره 

صفحات  -

تاریخ انتشار 2001