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PubMed1999

Reversible Kupffer cell suppression in biliary obstruction is caused by hydrophobic bile acids.

BACKGROUND/AIM: Biliary obstruction is associated with suppressed Kupffer cell clearance of bacteria and intracellular bactericidal activity of the phagocytes. We studied the superoxide generation of Kupffer cell in biliary obstruction and after incubation with bile acids to elucidate the mechanism of impaired intracellular killing of these phagocytes. METHODS: Kupffer cells were extracted from rats with common bile duct ligation or sham-operation. The extracted cells were tested for superoxide production immediately after extraction, 2 h and 24 h post-extraction. Superoxide generation from Kupffer cells after incubation with five bile acids (cholic acid, taurocholic acid, deoxycholic acid, chenodeoxycholic acid and ursodeoxycholic acid) at two different concentrations (0.1 mM and 1.0 mM) were also studied. Cell viability was monitored by trypan blue exclusion. RESULTS: Kupffer cells extracted from common duct-ligated animals had significantly lower superoxide production (-1.37+/-0.24 nmol O2(-)/10(6) cells) compared to that from sham-operated rats (2.54+/-0.58 nmol O2(-)/10(6) cells) and non-operated rats (2.15+/-0.76 nmol O2(-)/10(6) cells) (p<0.05). After 2 h of resting in culture medium, these cells recovered significantly in superoxide production to 2.72+/-0.63 nmol O2(-)/10(6) cells (p<0.01). A dose-related reduction in superoxide production was demonstrated when Kupffer cells were incubated with bile acids. Hydrophobic bile acids (deoxycholic acid and chenodeoxycholic acid) caused more significant suppression than with hydrophilic bile acids (cholic acid, taurocholic acid, ursodeoxycholic acid). The drop in superoxide production after bile acid treatment was not due to cell death. Washing in Hank's balanced salt solution resulted in partial recovery of Kupffer cell superoxide production. CONCLUSION: High blood levels of hydrophobic bile acids are likely to be the cause of impaired intracellular bactericidal activity of Kupffer cells in biliary obstruction.

Animals↗
PubMed1994

Peroxisome proliferation of hepatocytes in rats by a microbial degradation product of cholic acid, 4-(decahydro-6-methyl-3-oxocyclopenta(f)quinoline-7-yl)valeric acid.

Three-week oral administration of 4-(decahydro-6-methyl-3-oxo-cyclopenta(f)quinoline-7-yl)valeric acid (32-1328) in the diet supplemented at concentrations of 0.1% or 0.3% was associated with hepatomegaly and hypotriglyceridemia in male F344 rats. Electron microscopic examination of the liver revealed a remarkable increase of peroxisomes in hepatocytes both in number and size. Biochemically, there were increased activities of peroxisomal marker enzymes including the heat-labile enoyl-CoA hydratase and catalase while the mitochondrial enoyl-CoA hydratase activity was unchanged after feeding of 32-1328. These findings indicate that 32-1328 can exert peroxisome-proliferating activity to rat liver in a manner similar to typical peroxisome proliferators such as clofibrate or di(2-ethylhexyl)phthalate.

Animals↗