Effect of chronic ethanol feeding on kupffer cell-mediated antitumor cell activity

Shinzo Kato, Iwao Kurose, Hajime Higuchi, Hirotoshi Ebinuma, Hidetsugu Saito, Soichiro Miura, Hiromasa Ishii

研究成果: Article

3 引用 (Scopus)

抄録

We have previously reported that the Kupffer cell has antitumor activity through mitochondrial damage to tumor cells by nitric oxide production. In this study, the effect of chronic ethanol feeding on antihepatoma cell activity of the Kupffer cell was examined in rats. Male rats of the Wistar strain were fed ethanol chronically for 8 weeks by liquid diets. Kupffer cells were isolated from the control rat or the ethanol-fed rat, and cocultured with AH 70 cells, a rat hepatoma cell line. Fluorescence of rhodamine 123 or propidium iodide was observed as indicators of the mitochondrial damage or cell membrane injury, respectively, by a laser scanning confocal microscopy. Mitochondrial damage of AH 70 cells as indicated by reduction of rhodamine 123 fluorescence was smaller by the coculture with Kupffer cell from the ethanol rat than that from the control. Cell membrane barrier dysfunction of AH 70 cell was less frequently observed with the Kupffer cell from ethanol-fed rats. A metabolite of nitric oxide (nitrite and nitrate) was less in the cultured medium with the ethanol Kupffer cell than with the control Kupffer cell. Ca2+ mobilization, which induces inducible nitric oxide synthase and observed by the fluorescence of fluo-3, in Kupffer cells cocultured with AH 70 cells was suppressed in ethanol-fed rats. These result suggests that chronic ethanol feeding suppresses antrtumor cell activity of Kupffer cell through the impairment of Ca2+ mobilization and nitric oxide production.

元の言語English
ジャーナルAlcoholism: Clinical and Experimental Research
20
発行部数1 SUPPL.
出版物ステータスPublished - 1996

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Kupffer Cells
Ethanol
Rats
Rhodamine 123
Nitric Oxide
Fluorescence
Cell membranes
Cells
Rat control
Cell Membrane
Propidium
Confocal microscopy
Mitochondrial Membranes
Nitric Oxide Synthase Type II
Nutrition
Metabolites
Nitrites
Coculture Techniques
Confocal Microscopy
Nitrates

ASJC Scopus subject areas

  • Medicine (miscellaneous)
  • Toxicology

これを引用

Effect of chronic ethanol feeding on kupffer cell-mediated antitumor cell activity. / Kato, Shinzo; Kurose, Iwao; Higuchi, Hajime; Ebinuma, Hirotoshi; Saito, Hidetsugu; Miura, Soichiro; Ishii, Hiromasa.

:: Alcoholism: Clinical and Experimental Research, 巻 20, 番号 1 SUPPL., 1996.

研究成果: Article

Kato, Shinzo ; Kurose, Iwao ; Higuchi, Hajime ; Ebinuma, Hirotoshi ; Saito, Hidetsugu ; Miura, Soichiro ; Ishii, Hiromasa. / Effect of chronic ethanol feeding on kupffer cell-mediated antitumor cell activity. :: Alcoholism: Clinical and Experimental Research. 1996 ; 巻 20, 番号 1 SUPPL.
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abstract = "We have previously reported that the Kupffer cell has antitumor activity through mitochondrial damage to tumor cells by nitric oxide production. In this study, the effect of chronic ethanol feeding on antihepatoma cell activity of the Kupffer cell was examined in rats. Male rats of the Wistar strain were fed ethanol chronically for 8 weeks by liquid diets. Kupffer cells were isolated from the control rat or the ethanol-fed rat, and cocultured with AH 70 cells, a rat hepatoma cell line. Fluorescence of rhodamine 123 or propidium iodide was observed as indicators of the mitochondrial damage or cell membrane injury, respectively, by a laser scanning confocal microscopy. Mitochondrial damage of AH 70 cells as indicated by reduction of rhodamine 123 fluorescence was smaller by the coculture with Kupffer cell from the ethanol rat than that from the control. Cell membrane barrier dysfunction of AH 70 cell was less frequently observed with the Kupffer cell from ethanol-fed rats. A metabolite of nitric oxide (nitrite and nitrate) was less in the cultured medium with the ethanol Kupffer cell than with the control Kupffer cell. Ca2+ mobilization, which induces inducible nitric oxide synthase and observed by the fluorescence of fluo-3, in Kupffer cells cocultured with AH 70 cells was suppressed in ethanol-fed rats. These result suggests that chronic ethanol feeding suppresses antrtumor cell activity of Kupffer cell through the impairment of Ca2+ mobilization and nitric oxide production.",
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AU - Kato, Shinzo

AU - Kurose, Iwao

AU - Higuchi, Hajime

AU - Ebinuma, Hirotoshi

AU - Saito, Hidetsugu

AU - Miura, Soichiro

AU - Ishii, Hiromasa

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N2 - We have previously reported that the Kupffer cell has antitumor activity through mitochondrial damage to tumor cells by nitric oxide production. In this study, the effect of chronic ethanol feeding on antihepatoma cell activity of the Kupffer cell was examined in rats. Male rats of the Wistar strain were fed ethanol chronically for 8 weeks by liquid diets. Kupffer cells were isolated from the control rat or the ethanol-fed rat, and cocultured with AH 70 cells, a rat hepatoma cell line. Fluorescence of rhodamine 123 or propidium iodide was observed as indicators of the mitochondrial damage or cell membrane injury, respectively, by a laser scanning confocal microscopy. Mitochondrial damage of AH 70 cells as indicated by reduction of rhodamine 123 fluorescence was smaller by the coculture with Kupffer cell from the ethanol rat than that from the control. Cell membrane barrier dysfunction of AH 70 cell was less frequently observed with the Kupffer cell from ethanol-fed rats. A metabolite of nitric oxide (nitrite and nitrate) was less in the cultured medium with the ethanol Kupffer cell than with the control Kupffer cell. Ca2+ mobilization, which induces inducible nitric oxide synthase and observed by the fluorescence of fluo-3, in Kupffer cells cocultured with AH 70 cells was suppressed in ethanol-fed rats. These result suggests that chronic ethanol feeding suppresses antrtumor cell activity of Kupffer cell through the impairment of Ca2+ mobilization and nitric oxide production.

AB - We have previously reported that the Kupffer cell has antitumor activity through mitochondrial damage to tumor cells by nitric oxide production. In this study, the effect of chronic ethanol feeding on antihepatoma cell activity of the Kupffer cell was examined in rats. Male rats of the Wistar strain were fed ethanol chronically for 8 weeks by liquid diets. Kupffer cells were isolated from the control rat or the ethanol-fed rat, and cocultured with AH 70 cells, a rat hepatoma cell line. Fluorescence of rhodamine 123 or propidium iodide was observed as indicators of the mitochondrial damage or cell membrane injury, respectively, by a laser scanning confocal microscopy. Mitochondrial damage of AH 70 cells as indicated by reduction of rhodamine 123 fluorescence was smaller by the coculture with Kupffer cell from the ethanol rat than that from the control. Cell membrane barrier dysfunction of AH 70 cell was less frequently observed with the Kupffer cell from ethanol-fed rats. A metabolite of nitric oxide (nitrite and nitrate) was less in the cultured medium with the ethanol Kupffer cell than with the control Kupffer cell. Ca2+ mobilization, which induces inducible nitric oxide synthase and observed by the fluorescence of fluo-3, in Kupffer cells cocultured with AH 70 cells was suppressed in ethanol-fed rats. These result suggests that chronic ethanol feeding suppresses antrtumor cell activity of Kupffer cell through the impairment of Ca2+ mobilization and nitric oxide production.

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KW - Hepatoma

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KW - Mitochondria

KW - Nitric oxide

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