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Tumor necrosis factor-α regulates in vivo nitric oxide synthesis and induces liver injury during endotoxemia

✍ Scribed by Brian G. Harbrecht; Mauricio Di Silvio; A. J. Demetris; Richard L. Simmons; Timothy R. Billiar

Publisher
John Wiley and Sons
Year
1994
Tongue
English
Weight
688 KB
Volume
20
Category
Article
ISSN
0270-9139

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✦ Synopsis

Tumor necrosis factor-alpha is a principal mediator of the pathophysiological effects of endotoxemia and endotoxin shock. Tumor necrosis factor-a also contributes to the stimulation of nitric oxide synthesis by the induction of the enzyme nitric oxide synthase in a variety of tissues. Although the importance of tumor necrosis factor-a in the induction of nitric oxide synthase activity in uitro is well known, its role in in uiuo nitric oxide synthesis has not been convincingly established. We were interested in determining whether tumor necrosis factor-a plays a significant role in the in uiuo induction of nitric oxide synthesis. In Corynebacterium paruum-primed mice, lipopolysaccharide injection resulted in elevated serum tumor necrosis factor-a levels early and increased hepatic enzyme release (641 * 80 IU ASTL; 22.7 * 1.9 IU ornithine carbamoyltransferase per liter) and plasma nitrite and nitrate (804 * 84 pmol/L) 5 hr after lipopolysaccharide injection. Polyclonal rabbit antimouse anti-tumor necrosis factor-a reduced in uiuo tumor necrosis factor-a levels (1 hr, 7,332 rt 1,492 U tumor necrosis factor-a per milliliter) and reduced nitric oxide synthesis as measured by plasma nitrite and nitrate (352 rt 69 pmolb). Polyclonal rabbit antimouse anti-tumor necrosis factor-a also reduced lipopolysaccharide-induced hepatic enzyme release (428 2 33 IU AST/L; 16.0 2 2.5 JU ornithine carbamoyltransferase per liter). NG-monomethyl-L-arginine, a competitive inhibitor of nitric oxide synthesis, also decreased plasma nitrite and nitrate (104 * 9 pmol/L) but increased the lipopolysaccharide-induced hepatic injury (797 66 IU ASTD, 33.1 rt 2.1 IU ornithine carbamoyltransferase per liter). These results show that tumor necrosis factor-not only acts as an in uiuo signal for the induction of nitric oxide synthesis but

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