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

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Tolerance against tumor necrosis factor alpha (TNF)-induced hepatotoxicity in mice: the role of nitric oxide. / Bohlinger, I; Leist, M; Barsig, J; Uhlig, S; Tiegs, Gisa; Wendel, A.

in: TOXICOL LETT, Jahrgang 82-83, 1995, S. 227-231.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Bohlinger, I, Leist, M, Barsig, J, Uhlig, S, Tiegs, G & Wendel, A 1995, 'Tolerance against tumor necrosis factor alpha (TNF)-induced hepatotoxicity in mice: the role of nitric oxide.', TOXICOL LETT, Jg. 82-83, S. 227-231. <http://www.ncbi.nlm.nih.gov/pubmed/8597057?dopt=Citation>

APA

Bohlinger, I., Leist, M., Barsig, J., Uhlig, S., Tiegs, G., & Wendel, A. (1995). Tolerance against tumor necrosis factor alpha (TNF)-induced hepatotoxicity in mice: the role of nitric oxide. TOXICOL LETT, 82-83, 227-231. http://www.ncbi.nlm.nih.gov/pubmed/8597057?dopt=Citation

Vancouver

Bohlinger I, Leist M, Barsig J, Uhlig S, Tiegs G, Wendel A. Tolerance against tumor necrosis factor alpha (TNF)-induced hepatotoxicity in mice: the role of nitric oxide. TOXICOL LETT. 1995;82-83:227-231.

Bibtex

@article{f79b260b6abe402c86d9cb5a87b2dfc5,
title = "Tolerance against tumor necrosis factor alpha (TNF)-induced hepatotoxicity in mice: the role of nitric oxide.",
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.",
keywords = "Animals, Male, Cells, Cultured, Mice, Mice, Inbred BALB C, Nitric Oxide Synthase/antagonists & inhibitors, Interleukin-1/pharmacology, Liver/*drug effects, Nitric Oxide/*physiology, Nitroprusside/pharmacology, Tumor Necrosis Factor-alpha/*toxicity, Animals, Male, Cells, Cultured, Mice, Mice, Inbred BALB C, Nitric Oxide Synthase/antagonists & inhibitors, Interleukin-1/pharmacology, Liver/*drug effects, Nitric Oxide/*physiology, Nitroprusside/pharmacology, Tumor Necrosis Factor-alpha/*toxicity",
author = "I Bohlinger and M Leist and J Barsig and S Uhlig and Gisa Tiegs and A Wendel",
year = "1995",
language = "English",
volume = "82-83",
pages = "227--231",
journal = "TOXICOL LETT",
issn = "0378-4274",
publisher = "Elsevier BV",

}

RIS

TY - JOUR

T1 - Tolerance against tumor necrosis factor alpha (TNF)-induced hepatotoxicity in mice: the role of nitric oxide.

AU - Bohlinger, I

AU - Leist, M

AU - Barsig, J

AU - Uhlig, S

AU - Tiegs, Gisa

AU - Wendel, A

PY - 1995

Y1 - 1995

N2 - 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.

AB - 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.

KW - Animals

KW - Male

KW - Cells, Cultured

KW - Mice

KW - Mice, Inbred BALB C

KW - Nitric Oxide Synthase/antagonists & inhibitors

KW - Interleukin-1/pharmacology

KW - Liver/drug effects

KW - Nitric Oxide/physiology

KW - Nitroprusside/pharmacology

KW - Tumor Necrosis Factor-alpha/toxicity

KW - Animals

KW - Male

KW - Cells, Cultured

KW - Mice

KW - Mice, Inbred BALB C

KW - Nitric Oxide Synthase/antagonists & inhibitors

KW - Interleukin-1/pharmacology

KW - Liver/drug effects

KW - Nitric Oxide/physiology

KW - Nitroprusside/pharmacology

KW - Tumor Necrosis Factor-alpha/toxicity

M3 - SCORING: Journal article

VL - 82-83

SP - 227

EP - 231

JO - TOXICOL LETT

JF - TOXICOL LETT

SN - 0378-4274

ER -