Kupffer cells mediate increased anoxic hepatocellular killing from hyperosmolarity by an oxygen- and prostaglandin-independent mechanism

Toxicology Letters

Volumn 117, Issue 1-2, 2000, Pages 95-100

  Oh, Ki Wan ^a,b   Currin, Robert T ^a   Lemasters, John J ^a  

^a UNIVERSITY OF NORTH CAROLINA SCHOOL OF MEDICINE   (United States)

^b Chungbuk National University   (South Korea)

Author keywords

Anoxia hypoxia; Cell killing; Gadolinium chloride; Glycolysis; Hyperosmolarity; Indomethacin; Kupffer cells; Liver; Oxygen uptake; Prostaglandin

Indexed keywords

BUFFER; INDOMETACIN; PROSTAGLANDIN; PROSTAGLANDIN SYNTHASE;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL TISSUE; ANOXIA; ARTICLE; CONTROLLED STUDY; HYPEROSMOLARITY; KUPFFER CELL; LIVER CELL; NONHUMAN; OXYGEN CONSUMPTION; PRIORITY JOURNAL; PROSTAGLANDIN SYNTHESIS; RAT;

ANIMAL; ANOXIA; COMPARATIVE STUDY; EATING; FASTING; GADOLINIUM; GLYCOLYSIS; HEPATOCYTES; IN VITRO; INDOMETHACIN; KUPFFER CELLS; LACTATE DEHYDROGENASE; LIVER; MALE; OXYGEN; OXYGEN CONSUMPTION; PROSTAGLANDINS; RATS; RATS, SPRAGUE-DAWLEY; SALINE SOLUTION, HYPERTONIC; SUPPORT, U.S. GOV'T, P.H.S.; TIME FACTORS;

EID: 0034734831     PISSN: 03784274     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0378-4274(00)00247-2     Document Type: Article

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15. Modulation of tumor necrosis factor-alpha release by anisoosmolarity and betaine in rat liver macrophages (Kupffer cells)