PMID- 7625565
OWN - NLM
STAT- MEDLINE
DCOM- 19950829
LR  - 20190825
IS  - 0145-6008 (Print)
IS  - 0145-6008 (Linking)
VI  - 19
IP  - 2
DP  - 1995 Apr
TI  - Tumor necrosis factor-alpha cell-surface receptors of liver parenchymal and 
      nonparenchymal cells during acute and chronic alcohol administration to rats.
PG  - 332-8
AB  - Tumor necrosis factor-alpha (TNF-alpha) has been shown to contribute to the 
      alcohol [ethanol (ETOH)]-induced alteration of hepatic function. Therefore we 
      tested the hypothesis that the hepatic action of TNF-alpha could be due, at least 
      in part, to alterations in TNF-alpha cell-surface receptors of hepatic 
      parenchymal (hepatocytes) and nonparenchymal (Kupffer and sinusoidal endothelial) 
      cells. Rats were either acutely treated with ETOH by a primed, continuous 7-hr 
      intravenous infusion of 20% (w/v) ETOH (30 mg/100 g body weight/h) or chronically 
      fed an ETOH-containing liquid diet (5.2% ETOH, w/v, with ETOH as 36% of total 
      calories) for 14 weeks. Control rats in the acute group were infused with sterile 
      saline, whereas control rats in the chronic group were fed liquid diet containing 
      dextrin to replace ETOH in isocaloric amounts. Three hr before killing, the rats 
      were injected intravenously with Gram-negative bacterial lipopolysaccharide 
      [(LPS) 100 micrograms/100 g body weight] or saline. Hepatocytes, Kupffer cells, 
      and sinusoidal endothelial cells were isolated after liver perfusion with 
      collagenase (without pronase), separated by centrifugal elutriation, and used to 
      determine the affinity (Kd) and capacity (Bmax) of binding sites, using 
      recombinant human-[125I]TNF-alpha as the ligand. Two binding sites were detected 
      on Kupffer cells and sinusoidal endothelial cells isolated from control animals: 
      a high-affinity (Kd1, in the range of 150-200 pM), low-capacity (Bmax, in the 
      range of 2-3 fmol/10(6) cells) binding site and a low-affinity (Kd2, in the range 
      of 2-9 nM), high-capacity (Bmax2, in the range of 3-15 fmol/10(6) cells) binding 
      site.(ABSTRACT TRUNCATED AT 250 WORDS)
FAU - Deaciuc, I V
AU  - Deaciuc IV
AD  - Department of Physiology, Louisiana State University Medical Center, New Orleans 
      70112-1393, USA.
FAU - D'Souza, N B
AU  - D'Souza NB
FAU - Spitzer, J J
AU  - Spitzer JJ
LA  - eng
GR  - AA 09318/AA/NIAAA NIH HHS/United States
GR  - AA 09803/AA/NIAAA NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - England
TA  - Alcohol Clin Exp Res
JT  - Alcoholism, clinical and experimental research
JID - 7707242
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Receptors, Tumor Necrosis Factor)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Alcoholic Intoxication/*pathology
MH  - Alcoholism/*pathology
MH  - Animals
MH  - Dose-Response Relationship, Drug
MH  - Endothelium, Vascular/drug effects/pathology
MH  - Kupffer Cells/drug effects/pathology
MH  - Lipopolysaccharides/pharmacology
MH  - Liver/*drug effects/pathology
MH  - Male
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptors, Tumor Necrosis Factor/*drug effects/physiology
MH  - Tumor Necrosis Factor-alpha/*physiology
EDAT- 1995/04/01 00:00
MHDA- 1995/04/01 00:01
CRDT- 1995/04/01 00:00
PHST- 1995/04/01 00:00 [pubmed]
PHST- 1995/04/01 00:01 [medline]
PHST- 1995/04/01 00:00 [entrez]
AID - 10.1111/j.1530-0277.1995.tb01511.x [doi]
PST - ppublish
SO  - Alcohol Clin Exp Res. 1995 Apr;19(2):332-8. doi: 
      10.1111/j.1530-0277.1995.tb01511.x.