PMID- 10964098
OWN - NLM
STAT- MEDLINE
DCOM- 20001002
LR  - 20231213
IS  - 0143-3334 (Print)
IS  - 0143-3334 (Linking)
VI  - 21
IP  - 9
DP  - 2000 Sep
TI  - Prevention of the down-regulation of gap junctional intercellular communication 
      by green tea in the liver of mice fed pentachlorophenol.
PG  - 1671-6
AB  - Much evidence has been documented supporting the hypothesis that the 
      down-regulation of gap junctional intercellular communication (GJIC) is a 
      cellular event underlying the tumor promotion process and that treatment to 
      prevent the down-regulation or to up-regulate GJIC is important in preventing 
      tumor promotion. We explored the potential preventive effects of green tea 
      against the promoting action of pentachlorophenol (PCP) in mouse 
      hepatocarcinogenesis, examining whether drinking green tea prevents the 
      down-regulation of GJIC inhibition in the liver caused by tumorigenic doses of 
      PCP. We used a modified in vivo GJIC assay, the incision loading/dye transfer 
      method. Male B6C3F1 mice were given a green tea infusion for 1 week and then PCP 
      was fed at a dose of 300 or 600 p.p.m. in the diet for the following 2 weeks, 
      along with green tea treatment. A dose-related inhibition of GJIC in the 
      hepatocytes was evident in the mice treated with PCP alone that was associated 
      with a reduction in connexin32 (Cx32) plaques in the plasma membrane and an 
      increase in the cell proliferation index. Drinking green tea significantly 
      protected mice against GJIC inhibition, the reduction in Cx32 and the elevation 
      of the labeling index. These findings suggest that green tea might act as an 
      anti-promoter against PCP-induced mouse hepatocarcinogenesis via its ability to 
      prevent down-regulation of GJIC.
FAU - Sai, K
AU  - Sai K
AD  - Division of Cellular and Molecular Toxicology and Division of Risk Assessment, 
      National Institute of Health Sciences, 1-18-1 Kamiyohga, Setagayaku, Tokyo 
      158-8501, Japan.
FAU - Kanno, J
AU  - Kanno J
FAU - Hasegawa, R
AU  - Hasegawa R
FAU - Trosko, J E
AU  - Trosko JE
FAU - Inoue, T
AU  - Inoue T
LA  - eng
GR  - P42ES04911/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - England
TA  - Carcinogenesis
JT  - Carcinogenesis
JID - 8008055
RN  - 0 (Anticarcinogenic Agents)
RN  - 0 (Carcinogens)
RN  - 0 (Connexins)
RN  - 0 (Fluorescent Dyes)
RN  - 0 (Tea)
RN  - D9BSU0SE4T (Pentachlorophenol)
SB  - IM
MH  - Animals
MH  - Anticarcinogenic Agents/*pharmacology/therapeutic use
MH  - Carcinogens/*toxicity
MH  - Cell Communication/*drug effects
MH  - Cell Division/drug effects
MH  - Connexins/metabolism
MH  - Down-Regulation/drug effects
MH  - Fluorescent Dyes
MH  - Gap Junctions/*drug effects
MH  - Liver/*cytology/drug effects
MH  - Liver Neoplasms, Experimental/chemically induced/pathology/prevention & control
MH  - Male
MH  - Mice
MH  - Mice, Inbred Strains
MH  - Pentachlorophenol/antagonists & inhibitors/*toxicity
MH  - *Phytotherapy
MH  - Tea/*therapeutic use
MH  - Gap Junction beta-1 Protein
EDAT- 2000/08/30 11:00
MHDA- 2000/10/07 11:01
CRDT- 2000/08/30 11:00
PHST- 2000/08/30 11:00 [pubmed]
PHST- 2000/10/07 11:01 [medline]
PHST- 2000/08/30 11:00 [entrez]
AID - 10.1093/carcin/21.9.1671 [doi]
PST - ppublish
SO  - Carcinogenesis. 2000 Sep;21(9):1671-6. doi: 10.1093/carcin/21.9.1671.