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1 Laboratory of Hepatobiology
and Toxicology,
The relationship
among gender, lipopolysaccharide (LPS), and liver disease is complex.
Accordingly, the effect of estrogen on activation of Kupffer cells by
endotoxin was studied. All rats given estrogen intraperitoneally 24 h
before an injection of a sublethal dose of LPS (5 mg/kg) died
within 24 h, whereas none of the control rats died. Mortality was
prevented totally by pretreatment with gadolinium chloride, a Kupffer
cell toxicant. Peak serum tumor necrosis factor-
(TNF-) values as
well as TNF- mRNA in the liver after LPS were twice as high in the
estrogen-treated group as in the untreated controls. Plasma nitrite
levels and inducible nitric oxide synthase in the liver were also
elevated significantly in estrogen-treated rats 6 h after LPS.
Furthermore, Kupffer cells isolated from estrogen-treated rats produced
about twice as much TNF- and nitrite as controls did in response to LPS. In addition, Kupffer cells from estrogen-treated rats required 15-fold lower amounts of LPS to increase intracellular
Ca2+ than controls did, and
Kupffer cells from estrogen-treated animals expressed more CD14, the
receptor for LPS/LPS binding protein, than controls. Moreover, estrogen
treatment increased LPS binding protein mRNA dramatically in liver in
6-24 h. It is concluded that estrogen treatment in vivo sensitizes
Kupffer cells to LPS, leading to increased toxic mediator production by
the liver.
lipopolysaccharide; tumor necrosis factor-; nitric oxide; intracellular calcium; CD14
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