Reduced stress defense in heme oxygenase 1-deficient cells.

Journal Article (Journal Article)

Stressed mammalian cells up-regulate heme oxygenase 1 (Hmox1; EC, which catabolizes heme to biliverdin, carbon monoxide, and free iron. To assess the potential role of Hmox1 in cellular antioxidant defense, we analyzed the responses of cells from mice lacking functional Hmox1 to oxidative challenges. Cultured Hmox1(-/-) embryonic fibroblasts demonstrated high oxygen free radical production when exposed to hemin, hydrogen peroxide, paraquat, or cadmium chloride, and they were hypersensitive to cytotoxicity caused by hemin and hydrogen peroxide. Furthermore, young adult Hmox1(-/-) mice were vulnerable to mortality and hepatic necrosis when challenged with endotoxin. Our in vitro and in vivo results provide genetic evidence that up-regulation of Hmox1 serves as an adaptive mechanism to protect cells from oxidative damage during stress.

Full Text

Duke Authors

Cited Authors

  • Poss, KD; Tonegawa, S

Published Date

  • September 30, 1997

Published In

Volume / Issue

  • 94 / 20

Start / End Page

  • 10925 - 10930

PubMed ID

  • 9380736

Pubmed Central ID

  • PMC23533

International Standard Serial Number (ISSN)

  • 0027-8424

Digital Object Identifier (DOI)

  • 10.1073/pnas.94.20.10925


  • eng

Conference Location

  • United States