“…In the last several years, several studies have been published, showing a protective effect of nitric oxide in a variety of paradigms of cell injury and cell death. These include (1) direct scavenging of free radicals (Hogg et al, 1993 ; Wink et al, 1993) ; (2) effects on intracellular iron metabolism, including interaction with iron to form nitrosyl‐iron complexes (Rauhala et al., 1996 ; Sergent et al, 1997 ; Yoshie and Ohshima, 1997), preventing release of iron from ferritin (Puntarulo and Cederbaum, 1997), or stimulating iron‐responsive RNA binding elements such as cis ‐aconitase (Jaffrey et al, 1994) ; (3) inactivation of caspases (Dimmeler et al, 1997) ; (4) activation of a cyclic GMP‐dependent survival pathway, as has been seen in PC12 cells (Farinelli et al, 1996) and tumor necrosis factor‐α‐induced apoptosis in endothelial cells (Polte et al, 1997) ; (5) inducing expression of protective proteins such as heat shock proteins (Kim et al, 1997) ; (6) inhibition of nuclear factor‐κB activation (Peng et al, 1995 ; Matthews et al, 1996 ; Park et al, 1997 ; Togashi et al, 1997) ; (7) inhibition of glyceradehyde‐3‐phosphate dehydrogenase (Dimmeler et al, 1992 ; Kots et al, 1992 ; Molina y Vedia et al, 1992 ; McDonald and Moss, 1993 ; Itoga et al, 1997), whose activity appears to be required in one paradigm of neuronal apoptosis (Ishitani et al, 1996) ; and (8) oxidation in neurons of a redox modulatory site on the NMDA receptor, resulting in a decrease in NMDA receptor‐mediated currents (Lei et al, 1992), a mechanism that remains controversial (Aizenman et al, 1998).…”