Advertisement
Research Article Free access | 10.1172/JCI107599
Department of Medicine, University of California, San Francisco, California 94143, USA.
Find articles by Gemsa, D. in: PubMed | Google Scholar
Department of Medicine, University of California, San Francisco, California 94143, USA.
Find articles by Woo, C. in: PubMed | Google Scholar
Department of Medicine, University of California, San Francisco, California 94143, USA.
Find articles by Fudenberg, H. in: PubMed | Google Scholar
Department of Medicine, University of California, San Francisco, California 94143, USA.
Find articles by Schmid, R. in: PubMed | Google Scholar
Published February 1, 1974 - More info
In rat peritoneal macrophages, engaged in erythrophagocytosis in vitro, endotoxin stimulated heme oxygenase (HO) activity, which was additive to the substrate-mediated enzyme induction produced by the ingested erythrocyte hemoglobin. Endotoxin neither appeared to injure the erythrocytes, nor did it enhance the rate of erythrophagocytosis. In intact rats, HO activity in both parenchymal and sinusoidal cells of the liver was increased after treatment with endotoxin. It is likely that endotoxin directly stimulates HO activity, a process which may account for the reported rise in bilirubin formation in endotoxin-treated animals. The effect of endotoxin on HO may represent part of the general activation of phagocytic cells by endotoxin.