Nitric oxide.

Once activated by agents such as IFN-y and bacterial LPS, macrophages (MO)t can inhibit the growth of a wide variety of tumor and microbial targets (1, 2) . Although MO products such as hydrogen peroxide, TNFa, and IL-1 cause cytostasis and/or cytotoxicity (3-5), in many cases these mediators do not appear to be involved . With some targets, Mo-mediated cytostasis and injury to the mitochondria) electron transport chain (METC) require a process associated with MO oxidation of the guanido nitrogens of L-arginine to N02 -/NO3 (6). However, it is unknown if a metabolite of L-arginine causes these injuries, and if so, which metabolite. Activated Mo have recently been shown to release a compound similar to or identical with the reactive radical nitric oxide (NO .) during metabolism of L-arginine to N02 -/NO3 (7) . This report identifies NO. (or a closely related product) as a mediator of MO-induced cytostasis and mitochondria) respiratory inhibition in lymphoma cells .