Effect of Endogenous Nitric Oxide on Mitochondrial Respiration of Rat Hepatocytes In Vitro and In Vivo

doi:10.1001/archsurg.1991.01410260074010

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Vol. 126 No. 2, February 1991

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PAPERS READ BEFORE THE TENTH ANNIVERSARY MEETING OF THE SURGICAL INFECTION SOCIETY, CINCINNATI, OHIO, June 14 to 16, 1990-PART II

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Effect of Endogenous Nitric Oxide on Mitochondrial Respiration of Rat Hepatocytes In Vitro and In Vivo

Josef Stadler, MD; Ronald D. Curran, MD; Juan B. Ochoa, MD; Brian G. Harbrecht, MD; Rosemary A. Hoffman; Richard L. Simmons, MD; Timothy R. Billiar, MD

Arch Surg. 1991;126(2):186-191.

Abstract

• Nitric oxide, a highly reactive radical, was recentlyidentified as an intermediate of L-arginine metabolism in mammaliancells. We have shown that nitric oxide synthesis is inducedin vitro in cultured hepatocytes by supernatants from activatedKupffer cells or in vivo by injecting rats with nonviable Corynebacteriumparvum. In both cases, nitric oxide biosynthesis in hepatocyteswas associated with suppression of total protein synthesis.This study attempts to determine the effect of nitric oxidebiosynthesis on the activity of specific hepatocytic mitochondrialenzymes and to determine whether inhibition of protein synthesisis caused by suppression of energy metabolism. Exposure of hepatocytesto supernatants from activated Kupffer cells led to a 30% decreaseof aconitase (Krebs cycle) and complex I (mitochondrial electrontransport chain) activity. Using N^G-monomethyl-L-arginine, aninhibitor of nitric oxide synthesis, we demonstrated that theInhibition of mitochondrial aconitase activity was due, in part,to the action of nitric oxide. In contrast, in vivo nitric oxidesynthesis of hepatocytes from Corynebacterium parvum–treatedanimals had no effect on mitochondrial respiration. This suggeststhat inhibition of protein synthesis by nitric oxide is notlikely to be mediated by inhibition of energy metabolism.

(Arch Surg. 1991;126:186-191)

Author Affiliations

From the Department of Surgery, University of Pittsburgh (Pa).

Footnotes

Accepted for publication November 20, 1990.

Read before the Tenth Anniversary Meeting of the Surgical InfectionSociety, Cincinnati, Ohio, June 14, 1990.

Reprint requests to Department of Surgery, University of Pittsburgh,497 Scaife Hall, Pittsburgh, PA 15261 (Dr Stadler).

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