Inhibition of metabolic cooperation by the anticonvulsants, diphenylhydantoin and phenobarbital

Jone, Cyrenius M.; Erickson, Laurie; Trosko, James E.; Netzloff, Michael L.; Chang, Chia‐Cheng

doi:10.1002/tcm.1770050602

Cited by 16 publications

(2 citation statements)

References 72 publications

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“…Stock solutions of phenytoin (50 mM) were prepared in 100% ethanol (cf. Jone et al, 1985) and diluted in DMEM to final concentrations. Cell cultures were maintained at 37°C in an atmosphere of 94% air and 6% CO,.…”

Section: Introductionmentioning

confidence: 99%

Cytochrome P450 in rat astrocytes in vivo and in vitro: Intracellular localization and induction by phenytoin

Kempermann

Knoth

Gebicke‐Haerter

et al. 1994

J of Neuroscience Research

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Cytochrome P450IIB1,2 (nomenclature according to Nelson et al., DNA Cell Biol 12:1-51, 1993 and Volk et al., Neuroscience 42:215-235, 1991) immunoreactivity (P450-IR) is associated with astrocytes both in vivo and in vitro. Although they are unevenly distributed throughout the brain with a preference for phylogenetically elder parts, no significant differences between astrocytes prepared from different brain regions were observed in astrocyte cultures. The percentage of strongly immunoreactive astrocytes decreased from 40% after 7 days in culture to 15% after 21 days. Essentially all astrocytes have a low but significant P450-IR within this interval. Preembedding immunoelectron microscopy revealed peroxidase reaction products on the endoplasmic reticulum and on the outer membranes of mitochondrial and nuclear envelopes. Phenytoin (1 microM) added to the medium for 7 days significantly (1.22-fold) increased the amount of total P450 in astrocyte homogenates as measured by spectrophotometry. Considerably more immunoreactive cells (1.5-fold) were found in treated cultures than in controls.

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Section: Introductionmentioning

confidence: 99%

Cytochrome P450 in rat astrocytes in vivo and in vitro: Intracellular localization and induction by phenytoin

Kempermann

Knoth

Gebicke‐Haerter

et al. 1994

J of Neuroscience Research

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“…Phenobarbital inhibited intercellular communication between Chinese hamster V79 cells (Jone et al, 1986) and between primary cultured rat hepatocytes and ARL liver epithelial cells (Williams, 1980(Williams, , 1981. In contrast, Umeda et al (1980) reported no effect of phenobarbital on intercellular communication between V79 cells.…”

Section: Discussionmentioning

confidence: 94%

Effects of tumor promoters, genotoxic carcinogens and hepatocytotoxins on mouse hepatocyte intercellular communication

Ruch

Klaunig

1986

Cell Biol Toxicol

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Intercellular communication via gap junctions may be an important mechanism of cellular growth control. Tumor promoters can inhibit intercellular communication between cultured cells, while genotoxic carcinogens apparently lack this capability. The inhibition of intercellular communication by tumor promoters may be an essential mechanism by which tumor promotion occurs in vivo. In this study, the liver tumor promoters phenobarbital, lindane (1,2,3,4,5,6-hexachlorocyclohexane, gamma-isomer), DDT (1,1-Bis[4-chlorophenyl]-2,2,2-trichloroethane), Aroclor 1254 (a polychlorinated biphenyl mixture) and dieldrin inhibited intercellular communication between male B6C3F1 mouse hepatocytes in primary culture. Intercellular communication was detected as the passage of [5-3H]uridine nucleotides from pre-labelled donor hepatocytes to non-labelled recipient hepatocytes. Mouse hepatocyte intercellular communication was also inhibited by the skin tumor promoter TPA (12-0-tetradecanoyl-phorbol-13-acetate), but not by the bladder tumor promoter saccharin. The genotoxic hepatocarcinogens dimethylnitrosamine, diethylnitrosamine, benzo[a]pyrene and 2-acetylaminofluorene, and the hepatocytotoxins bromobenzene, acetaminophen, carbon tetrachloride, chloroform and methotrexate had no effect on mouse hepatocyte intercellular communication at non-cytotoxic levels. These results suggest that the ability to inhibit mouse hepatocyte intercellular communication is an effect specific to tumor promoters.

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Phenobarbital specifically reduces gap junction protein mRNA level in rat liver

Mesnil

Fitzgerald

Yamasaki

1988

Molecular Carcinogenesis

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The gene expression of liver major gap junction (GJ) protein was studied in rats systemically administered phenobarbital, a rat liver tumor promoter. Using a GJ protein cDNA and northern blot analysis, the level of GJ protein mRNA in liver was observed to be markedly reduced at 4 and 11 wk of phenobarbital exposure (0.1% in drinking water). However, the level of GJ protein mRNA was not altered in kidney at 11 wk of exposure. In liver, phenobarbital did not induce expression of the neoplasm-associated marker genes glutathione S-transferase (placental form) and gamma-glutamyltranspeptidase, while in kidney the observed expression of these genes was not changed. These in vivo results indicate that phenobarbital reduces GJ protein gene expression specifically in rat liver without altering expression of genes often altered during liver carcinogenesis, and they support assigning a role for the impairment of gap junctional intercellular communication in phenobarbital-mediated liver tumor promotion.

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Inhibition of metabolic cooperation by the anticonvulsants, diphenylhydantoin and phenobarbital

Cited by 16 publications

References 72 publications

Cytochrome P450 in rat astrocytes in vivo and in vitro: Intracellular localization and induction by phenytoin

Cytochrome P450 in rat astrocytes in vivo and in vitro: Intracellular localization and induction by phenytoin

Effects of tumor promoters, genotoxic carcinogens and hepatocytotoxins on mouse hepatocyte intercellular communication

Phenobarbital specifically reduces gap junction protein mRNA level in rat liver

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