Effects of Nitric Oxide (NO) Synthesis Inhibition on Antitumor Responses during Interleukin-2 (IL-2) Treatment of Mice
Objectives To evaluate if L-arginine: NO pathway is activated in tumor tissues during IL-2 therapy and to evaluate whether IL-2 induced NO synthesis represents an antitumor effector muchanism or an inhibitory factor against therapeutic effects of IL-2. Methods Four groups[untreated control, N G -monomethyl-L-arginine(MLA) therapy only, IL-2 therapy only, IL-2/MLA therapy groups] of BALB/c mice were injected intraperitoneally with 2×10 6 Meth A tumor cells on day 0. MLA was administered subcutaneously with Alzet continuous infusion pumps on day 2. IL-2 therapy (180,000 IU s.c. every 12h for 5 days) was started on day 3. NO production within ascites tumors was assessed by measuring nitrite concentrations in cultures of ascites cells harvested on day 8. Survival and the rate of body weight increment of the mice were measured to evaluate therapeutic responses. Daily urinary nitrate excretion was monitored to demonstrate the effectiveness of MLA in inhibiting NO synthesis. Results Nitrite production in supernatants of Meth A ascites cell cultures was 63±14 μM in IL-2 treated mice and 3.2±1.5 μM in untreated controls (p Conclusion L-arginine: NO pathway can be activated in malignant ascites, by IL-2 therapy and NO synthesis functions as an inhibitory mechanism against IL-2 induced anti-tumor effects.
- PubMed Central : 저널 > https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4532021
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