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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2004.9
- 수록면
- 50 - 56 (7page)
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The present study was designed to determine the impact of mercury on endotoxininduced
inflammatory cytokine expression and corresponding signal transduction in mouse kidney.
Male BALB/c mice were exposed continuously to 0, 0.3, 1.5, 7.5, or 37.5 ppm of mercury in drinking
water for 14 days and at the end of the treatment period, lipopolysaccharide (LPS, 0.5 mg/kg)
was injected intraperitoneally 2 h prior to euthanasia. The doses of mercury and LPS did not cause
hepatotoxicity or renal toxicity as indicated by unaltered plasma alanine aminotransferase and aspartate
aminotransferase levels, and terminal UTP nucleotide end-labeling assay from kidney, respectively.
Mercury decreased kidney glutathione (GSH) and with LPS, it additively decreased GSH.
Mercury activated p38 mitogen-activated protein kinase (MAPK) and additively increased LPSinduced
p38 MAPK phosphorylation. In contrast, mercury inhibited LPS-induced activation of extracellular
signal-regulated kinase (ERK) but had no effect alone. Mercury increased the gene expression
of tumor necrosis factor α (TNFα) and potentiated LPS-induced TNFα expression. Mercury did
not affect LPS-induced interleukin-1β (IL-1β) expression but decreased LPS-induced IL-6 expression.
These results suggest that low levels of mercury might augment LPS-induced TNFα expression
by altering GSH and p38 MAPK. Mercury modulates LPS-induced p38 and ERK activation, and
downstream TNFα and IL-6 expression in kidney, respectively.
inflammatory cytokine expression and corresponding signal transduction in mouse kidney.
Male BALB/c mice were exposed continuously to 0, 0.3, 1.5, 7.5, or 37.5 ppm of mercury in drinking
water for 14 days and at the end of the treatment period, lipopolysaccharide (LPS, 0.5 mg/kg)
was injected intraperitoneally 2 h prior to euthanasia. The doses of mercury and LPS did not cause
hepatotoxicity or renal toxicity as indicated by unaltered plasma alanine aminotransferase and aspartate
aminotransferase levels, and terminal UTP nucleotide end-labeling assay from kidney, respectively.
Mercury decreased kidney glutathione (GSH) and with LPS, it additively decreased GSH.
Mercury activated p38 mitogen-activated protein kinase (MAPK) and additively increased LPSinduced
p38 MAPK phosphorylation. In contrast, mercury inhibited LPS-induced activation of extracellular
signal-regulated kinase (ERK) but had no effect alone. Mercury increased the gene expression
of tumor necrosis factor α (TNFα) and potentiated LPS-induced TNFα expression. Mercury did
not affect LPS-induced interleukin-1β (IL-1β) expression but decreased LPS-induced IL-6 expression.
These results suggest that low levels of mercury might augment LPS-induced TNFα expression
by altering GSH and p38 MAPK. Mercury modulates LPS-induced p38 and ERK activation, and
downstream TNFα and IL-6 expression in kidney, respectively.
목차
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
ACKNOWLEDGEMENTS
REFERENCES
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UCI(KEPA) : I410-ECN-0101-2009-513-014287273