| Literature DB >> 7695603 |
S de Vos1, C J Epstein, E Carlson, S K Cho, H P Koeffler.
Abstract
Tumor necrosis factor is a key mediator of the septic shock syndrome, and its secretion by monocytes is induced by endotoxin. Increasing evidence exists that the release of oxygen-derived free radicals by polymorphonuclear cells plays a central role in tumor necrosis factor toxicity. Superoxide dismutases scavenge oxygen-derived free radicals and appear to be excellent candidates to provide protection against tumor-necrosis-factor -mediated cytotoxicity. In this study, we have found that transgenic mice overexpressing the human gene for CuZn SOD are not protected against experimentally induced endotoxemia.Entities:
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Year: 1995 PMID: 7695603 DOI: 10.1006/bbrc.1995.1370
Source DB: PubMed Journal: Biochem Biophys Res Commun ISSN: 0006-291X Impact factor: 3.575