Tolerance against tumor necrosis factor alpha (TNF)-induced hepatotoxicity in mice: the role of nitric oxide

Toxicology Letters
I BohlingerA Wendel

Abstract

D-Galactosamine-sensitized mice challenged with tumor necrosis factor alpha (TNF) developed severe apoptotic and secondary necrotic liver injury as assessed by histology, measurement of cytosolic DNA fragments and determination of liver-specific enzymes in plasma. Pretreatment of mice with interleukin-1 beta (IL-1) resulted in elevated levels of nitrite/nitrate in serum and rendered mice insensitive towards TNF toxicity. Pharmacological doses of the nitric oxide (NO) donor sodium nitroprusside (SNP) also conferred complete protection against TNF toxicity, suggesting a possible link between IL-1- and NO-induced protection. However, NO-synthesis inhibition by NG-monomethyl-L-arginine failed to abrogate IL-1-induced tolerance against TNF toxicity. We conclude that IL-1 and NO protect against TNF-induced liver injury through distinct pathways.

References

Nov 1, 1992·The Journal of Clinical Investigation·P J Shultz, L Raij
Jan 1, 1994·Cardiovascular Research·A PetrosP Vallance
Apr 15, 1993·Proceedings of the National Academy of Sciences of the United States of America·D A GellerT R Billiar

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Citations

Jul 10, 1999·Mechanisms of Ageing and Development·L E RikansT Yamano
Jan 4, 2001·International Journal of Immunopharmacology·M I LusterB Yucesoy
Feb 15, 2002·Toxicology·Dario C Ramirez, María S Gimenez
Apr 27, 2001·Toxicology Letters·M I LusterB Yucesoy
Nov 13, 1998·Proceedings of the National Academy of Sciences of the United States of America·R M RaiA M Diehl

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