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Manganese Superoxide Dismutase: A Hepatic Acute Phase Protein Regulated by Interleukin-6 and Glucocorticoids^*

WILLIAM C. DOUGALL and HARRY S. NICK

Department of Biochemistry and Molecular Biology, J. Hillis Miller Health Center, University of Florida College of Medicine Gainesville, Florida 32610

Address all correspondence and requests for reprints to: Dr. Harry S. Nick, Department of Biochemistry and Molecular Biology, University of Florida College of Medicine, Box J-245, Gainesville, Florida 32610.

Abstract

The superoxide dismutases (SODs) are important metallo-enzymes which scavenge and dismutate the superoxide free radical. They are thought to be the main enzymes in the antioxidant defense system. Identification of stimuli that control transcription of the SOD genes is essential for understanding SOD gene regulation. In this study we show that manganese SOD (MnSOD) mRNA levels are elevated by lipopolysaccharide, a bacterial endotoxin, in rat liver. However, neither lipopolysaccharide nor tumor necrosis factor- had an effect on MnSOD mRNA expression in cultured primary hepatocytes. On the other hand, the inflammatory cytokines, interleukin-1 (IL-1) and IL-6 did increase MnSOD mRNA levels, either 2- or 15-fold, respectively, over a 20-h period in hepatocytes. The IL-6-induced increase in MnSOD mRNA levels was attenuated by dexamethasone, a glucocorticoid, in hepatocytes cultured for less than 16 h. In contrast, in hepatocytes originally cultured for more than 16 h, IL-6 and dexamethasone produced a synergistic increase in MnSOD mRNA levels. The induction of MnSOD expression by IL-6, which is a known inflammatory cytokine, suggests that MnSOD may play a role in the inflammation process. Since inflammation is known to result in oxidative damage to cells, the role of MnSOD may be to protect cells from inflammation-mediated oxidative damage. (Endocrinology 129: 2376–2384, 1991)

Footnotes

^* This work was supported by NIH Grant RO1-KL39593 (to H.S.N.).

Current address: Division of Immunology, Department of Pathology, University of Pennsylvania, Philadelphia, Pennsylvania 19104.

Received March 29, 1991.

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