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.