Publication: Lack of promoting effect of proline on bile duct cancer development in dimethylnitrosamine‐initiated hamster livers
Issued Date
1994-01-01
Resource Type
ISSN
15206866
02703211
02703211
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2-s2.0-0028108038
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Mahidol University
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SCOPUS
Bibliographic Citation
Teratogenesis, Carcinogenesis, and Mutagenesis. Vol.14, No.4 (1994), 169-174
Suggested Citation
Witaya Thamavit, Chawalit Pairojkul, Danai Tiwawech, Tomoyuki Shirai, Nobuyuki Ito Lack of promoting effect of proline on bile duct cancer development in dimethylnitrosamine‐initiated hamster livers. Teratogenesis, Carcinogenesis, and Mutagenesis. Vol.14, No.4 (1994), 169-174. doi:10.1002/tcm.1770140403 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/9539
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Title
Lack of promoting effect of proline on bile duct cancer development in dimethylnitrosamine‐initiated hamster livers
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Abstract
Bile duct hyperplasia caused by proline is believed to represent a chemical effect of the liver fluke, Fasciola hepatica, and the resultant cell division might be expected to play a role as a tumor promoter. To investigate the potential promoting effect of proline on bile duct cancer development, Syrian hamsters were therefore divided into 8 treatment groups: dimethylnitrosamine (DMN) + proline intraperitoneally (i.p.); DMN + proline s.c.; DMN + saline i.p.; DMN + saline s.c.; proline i.p.; proline s.c.; saline i.p.; and saline s.c. DMN was injected i.p. at 20 mg/kg to the animals 2 weeks prior to commencement of proline treatment, whereby 1 ml of a 2 M solution was given by i.p. or s.c. injection 3 times a week for 20 weeks. At the end of week 42, assessment of preneoplastic lesion development did not reveal any significant modulating influence of proline on DMN‐initiated lesion development nor did it itself cause persistent bile duct hyperplasia. © 1994 Wiley‐Liss, Inc. Copyright © 1994 Wiley‐Liss, Inc., A Wiley Company