Effect of PCBs on mouse lung tumorigenesis induced by 1-nitropyrene: A preliminary report

Y. Nakanishi, F. Bai, K. Takayama, Xin-Hai Pei, K. Inoue, S. I. Osaki, M. Izumi, Y. Takaki, N. Hara, H. Tokiwa, Y. Masuda

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Abstract

We have analyzed the effect of polychlorinated biphenyls (PCB, Kanechlor 400) on 1-nitropyrene (1-NP) induced lung tumor. Male A/J mice (6 weeks old) were used for the experiment. A total of 2.5 mg/kg PCB was administered intraperitoneally (PCB group), a total of 0.38 mmol/kg 1-NP was administered intraperitoneally for 17 times (1-NP group), PCB was administered followed by ip injection of 1-NP (PCB + 1-NP group), and only vehicle was administered (control group). The lung lesions induced were examined 18 weeks after the final treatment with 1-NP or vehicle. In control group, no neoplastic lesion in the lung was induced. In PCB group, only one lesion with adenoma was induced. In 1-NP group, various kinds of lung neoplastic lesions including hyperplasia, adenoma and adenocarcinoma were induced. In PCB + 1-NP group, both the number and size of tumors induced were significantly more than those in 1-NP group. In addition, the number of adenocarcinoma formed was more in PCB + 1-NP group than in 1-NP group. Each lesion was microdissected to collect and analyze DNA of the targeted tissue. K-ras gene mutation was detected in part of adenoma lesions and all the carcinoma lesions. The mutation was found in either 1-NP or PCB + 1-NP group, but not in control and PCB group. The pattern of K-ras mutation was CAA to CGA in codon 61 or GGT to GAT in codon 12. There was no difference in the pattern of K-ras mutation despite of the pretreatment with PCB. Although the present data are from small sample size, it was suggested that PCB may promote (but not initiate) 1-NP induced lung tumorigenesis, and may not induce K-ras mutation directly in the experimental system.

Original languageEnglish (US)
Pages (from-to)231-237
Number of pages7
JournalFukuoka Acta Medica
Volume90
Issue number5
StatePublished - 1999
Externally publishedYes

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1-nitropyrene
Polychlorinated Biphenyls
Carcinogenesis
Lung
Mutation
Adenoma
Codon
Control Groups

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Nakanishi, Y., Bai, F., Takayama, K., Pei, X-H., Inoue, K., Osaki, S. I., ... Masuda, Y. (1999). Effect of PCBs on mouse lung tumorigenesis induced by 1-nitropyrene: A preliminary report. Fukuoka Acta Medica, 90(5), 231-237.

Effect of PCBs on mouse lung tumorigenesis induced by 1-nitropyrene : A preliminary report. / Nakanishi, Y.; Bai, F.; Takayama, K.; Pei, Xin-Hai; Inoue, K.; Osaki, S. I.; Izumi, M.; Takaki, Y.; Hara, N.; Tokiwa, H.; Masuda, Y.

In: Fukuoka Acta Medica, Vol. 90, No. 5, 1999, p. 231-237.

Research output: Contribution to journalArticle

Nakanishi, Y, Bai, F, Takayama, K, Pei, X-H, Inoue, K, Osaki, SI, Izumi, M, Takaki, Y, Hara, N, Tokiwa, H & Masuda, Y 1999, 'Effect of PCBs on mouse lung tumorigenesis induced by 1-nitropyrene: A preliminary report', Fukuoka Acta Medica, vol. 90, no. 5, pp. 231-237.
Nakanishi Y, Bai F, Takayama K, Pei X-H, Inoue K, Osaki SI et al. Effect of PCBs on mouse lung tumorigenesis induced by 1-nitropyrene: A preliminary report. Fukuoka Acta Medica. 1999;90(5):231-237.
Nakanishi, Y. ; Bai, F. ; Takayama, K. ; Pei, Xin-Hai ; Inoue, K. ; Osaki, S. I. ; Izumi, M. ; Takaki, Y. ; Hara, N. ; Tokiwa, H. ; Masuda, Y. / Effect of PCBs on mouse lung tumorigenesis induced by 1-nitropyrene : A preliminary report. In: Fukuoka Acta Medica. 1999 ; Vol. 90, No. 5. pp. 231-237.
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abstract = "We have analyzed the effect of polychlorinated biphenyls (PCB, Kanechlor 400) on 1-nitropyrene (1-NP) induced lung tumor. Male A/J mice (6 weeks old) were used for the experiment. A total of 2.5 mg/kg PCB was administered intraperitoneally (PCB group), a total of 0.38 mmol/kg 1-NP was administered intraperitoneally for 17 times (1-NP group), PCB was administered followed by ip injection of 1-NP (PCB + 1-NP group), and only vehicle was administered (control group). The lung lesions induced were examined 18 weeks after the final treatment with 1-NP or vehicle. In control group, no neoplastic lesion in the lung was induced. In PCB group, only one lesion with adenoma was induced. In 1-NP group, various kinds of lung neoplastic lesions including hyperplasia, adenoma and adenocarcinoma were induced. In PCB + 1-NP group, both the number and size of tumors induced were significantly more than those in 1-NP group. In addition, the number of adenocarcinoma formed was more in PCB + 1-NP group than in 1-NP group. Each lesion was microdissected to collect and analyze DNA of the targeted tissue. K-ras gene mutation was detected in part of adenoma lesions and all the carcinoma lesions. The mutation was found in either 1-NP or PCB + 1-NP group, but not in control and PCB group. The pattern of K-ras mutation was CAA to CGA in codon 61 or GGT to GAT in codon 12. There was no difference in the pattern of K-ras mutation despite of the pretreatment with PCB. Although the present data are from small sample size, it was suggested that PCB may promote (but not initiate) 1-NP induced lung tumorigenesis, and may not induce K-ras mutation directly in the experimental system.",
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T1 - Effect of PCBs on mouse lung tumorigenesis induced by 1-nitropyrene

T2 - A preliminary report

AU - Nakanishi, Y.

AU - Bai, F.

AU - Takayama, K.

AU - Pei, Xin-Hai

AU - Inoue, K.

AU - Osaki, S. I.

AU - Izumi, M.

AU - Takaki, Y.

AU - Hara, N.

AU - Tokiwa, H.

AU - Masuda, Y.

PY - 1999

Y1 - 1999

N2 - We have analyzed the effect of polychlorinated biphenyls (PCB, Kanechlor 400) on 1-nitropyrene (1-NP) induced lung tumor. Male A/J mice (6 weeks old) were used for the experiment. A total of 2.5 mg/kg PCB was administered intraperitoneally (PCB group), a total of 0.38 mmol/kg 1-NP was administered intraperitoneally for 17 times (1-NP group), PCB was administered followed by ip injection of 1-NP (PCB + 1-NP group), and only vehicle was administered (control group). The lung lesions induced were examined 18 weeks after the final treatment with 1-NP or vehicle. In control group, no neoplastic lesion in the lung was induced. In PCB group, only one lesion with adenoma was induced. In 1-NP group, various kinds of lung neoplastic lesions including hyperplasia, adenoma and adenocarcinoma were induced. In PCB + 1-NP group, both the number and size of tumors induced were significantly more than those in 1-NP group. In addition, the number of adenocarcinoma formed was more in PCB + 1-NP group than in 1-NP group. Each lesion was microdissected to collect and analyze DNA of the targeted tissue. K-ras gene mutation was detected in part of adenoma lesions and all the carcinoma lesions. The mutation was found in either 1-NP or PCB + 1-NP group, but not in control and PCB group. The pattern of K-ras mutation was CAA to CGA in codon 61 or GGT to GAT in codon 12. There was no difference in the pattern of K-ras mutation despite of the pretreatment with PCB. Although the present data are from small sample size, it was suggested that PCB may promote (but not initiate) 1-NP induced lung tumorigenesis, and may not induce K-ras mutation directly in the experimental system.

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