Transgenic mice overexpressing human copper/zinc-superoxide dismutase (Cu/Zn SOD) are not resistant to endotoxic shock.
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.
de Vos
S
S
Division of Hematology/Oncology, Cedars-Sinai Medical Center, UCLA School of Medicine 90048.
Epstein
C J
CJ
Carlson
E
E
Cho
S K
SK
Koeffler
H P
HP
D000818:Animals; D006801:Humans; D008070:Lipopolysaccharides / Q000633:toxicity; D008297:Male; D051379:Mice; D008822:Mice, Transgenic; D012772:Shock, Septic / Q000201:enzymology*; D013482:Superoxide Dismutase / Q000378:metabolism*
D008070:Lipopolysaccharides; D013482:Superoxide Dismutase