{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,1]],"date-time":"2026-05-01T20:22:06Z","timestamp":1777666926896,"version":"3.51.4"},"reference-count":27,"publisher":"SAGE Publications","issue":"1","license":[{"start":{"date-parts":[[1996,1,1]],"date-time":"1996-01-01T00:00:00Z","timestamp":820454400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Hum Exp Toxicol"],"published-print":{"date-parts":[[1996,1]]},"abstract":"1 Since the literature suggested a portion of the overall toxicity of cyanide (CN) may be affected by nitric oxide, we investigated a long acting NO releasing complex (diethy lamine\/nitric oxide (DEA\/NO)) which may exhibit vasodi latory as well as other nitric oxide effects to determine its ability to modify CN toxicity. Sodium nitrite, a vasodilator commonly used to treat cyanide toxicity thought to act by methemoglobin (MHb) formation, can be rapidly trans formed to nitric oxide (NO).<\/jats:p>\n \n 2 Mice (n=10 per dose) were administered one of five doses of sodium cyanide (NaCN) intraperitoneally (4.28,5.08,6.03,7.17 and 8.52 mg kg\n -1<\/jats:sup>\n ). DEA\/NO was given intravenously (20 mg kg\n -1<\/jats:sup>\n ) 2 min prior to NaCN. As a control, N\n G<\/jats:sup>\n -monomethyl-L-arginine (L-NMMA), which inhibits NO synthesis, was administered intravenously (70 mg kg\n -1<\/jats:sup>\n ) to mice, 3 min prior to DEA\/NO.\n <\/jats:p>\n \n 3 Before CN toxicity studies, we determined whether DEA\/NO was producing MHb by collecting tail vein blood from mice and measuring MHb levels. For example, 4 min after DEA\/NO administration (5,10, and 20 mg kg\n -1<\/jats:sup>\n ), MHb levels were 1.2 7 \u00b1 0.28%, 2.60 \u00b1 0.26% and 6.53 \u00b10.54% respectively. O\n 2<\/jats:sub>\n capacity was also decreased in a dose related manner. Carboxyhemoglobin or percent O\n 2<\/jats:sub>\n satura tion, on the other hand, was not significantly inhibited. The LD\n 50<\/jats:sub>\n increased from 5.75 \u00b1 0.026 (CN alone) to 7.66 \u00b1 0.021 mg kg\n -1<\/jats:sup>\n (CN+DEA\/NO) resulting in a protec tive ratio of 1.73.\n <\/jats:p>\n \n 4 Results suggest the following: (1) L-NMMA, which inhibits the synthesis of endogenous NO, appears to exacerbate the DEA\/NO (or exogenous NO) response; (2) DEA\/NO appears to reduce the toxicity of CN which suggests that a portion of CN toxicity may be affected by a NO component; and (3) low DEA\/NO doses may act via a direct effect while higher doses (40 mg kg\n -1<\/jats:sup>\n ) may allow for formation of a concentration of MHb which can bind CN to form cyanomethemoglobin and reduce the toxicity of CN.\n <\/jats:p>","DOI":"10.1177\/096032719601500103","type":"journal-article","created":{"date-parts":[[2008,12,24]],"date-time":"2008-12-24T01:08:04Z","timestamp":1230080884000},"page":"13-18","source":"Crossref","is-referenced-by-count":10,"title":["Cyanide toxicity in mice pretreated with diethylamine nitric oxide complex"],"prefix":"10.1177","volume":"15","author":[{"given":"S.I.","family":"Baskin","sequence":"first","affiliation":[{"name":"Pharmacology Division, US Army Medical Research Institute of Chemical Defense, Aberdeen Proving Ground, MD 21010, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"E.W.","family":"Nealley","sequence":"additional","affiliation":[{"name":"Pharmacology Division, US Army Medical Research Institute of Chemical Defense, Aberdeen Proving Ground, MD 21010, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"J.C.","family":"Lempka","sequence":"additional","affiliation":[{"name":"Pharmacology Division, US Army Medical Research Institute of Chemical Defense, Aberdeen Proving Ground, MD 21010, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"179","published-online":{"date-parts":[[1996,1,1]]},"reference":[{"key":"atypb1","unstructured":"Way JL et al. Methemoglobin formation in the treatment of acute cyanide intoxication . In: Ballantyne B, Marrs T, (Eds.), Clinical and Experimental Toxicology of Cyanides Bristol, England: John Wright and Sons, 1987, pp. 402-412."},{"key":"atypb2","first-page":"234","volume":"33","author":"Cucinell SA","year":"1974","journal-title":"Federation Proceedings"},{"key":"atypb3","doi-asserted-by":"publisher","DOI":"10.1002\/jat.2550050607"},{"key":"atypb4","doi-asserted-by":"publisher","DOI":"10.1021\/ic00216a003"},{"key":"atypb5","first-page":"1009","volume":"148","author":"Paulet G.","year":"1954","journal-title":"Compt Rend Seances Soc Biol Fil"},{"key":"atypb6","doi-asserted-by":"crossref","first-page":"285","DOI":"10.1007\/BF00244736","volume":"237","author":"Bastian G.","year":"1959","journal-title":"Naunyn-Schmied Arch Exp Pathol Pharmakol"},{"key":"atypb7","doi-asserted-by":"publisher","DOI":"10.1016\/0014-2999(69)90170-8"},{"key":"atypb8","doi-asserted-by":"crossref","first-page":"163","DOI":"10.1016\/S0022-3565(25)27958-7","volume":"161","author":"Sheehy M.","year":"1968","journal-title":"J Pharmacol Exp Therapeut"},{"key":"atypb9","doi-asserted-by":"publisher","DOI":"10.1016\/0006-2952(76)90397-X"},{"key":"atypb10","first-page":"196","volume":"45","author":"Baskin SI","year":"1986","journal-title":"Fed Proc"},{"key":"atypb11","doi-asserted-by":"publisher","DOI":"10.1002\/jat.2550100507"},{"key":"atypb12","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.53.5.557"},{"key":"atypb13","doi-asserted-by":"publisher","DOI":"10.1038\/327524a0"},{"key":"atypb14","doi-asserted-by":"publisher","DOI":"10.1021\/ic50175a008"},{"key":"atypb15","doi-asserted-by":"publisher","DOI":"10.2165\/00003088-198409030-00005"},{"key":"atypb16","doi-asserted-by":"publisher","DOI":"10.1038\/139548a0"},{"key":"atypb17","first-page":"662","volume":"31","author":"Smith RP","year":"1991","journal-title":"Sci"},{"key":"atypb18","doi-asserted-by":"publisher","DOI":"10.1096\/fasebj.3.9.2545495"},{"key":"atypb19","doi-asserted-by":"publisher","DOI":"10.1021\/jm00115a013"},{"key":"atypb20","doi-asserted-by":"publisher","DOI":"10.1055\/s-0038-1649644"},{"key":"atypb21","doi-asserted-by":"publisher","DOI":"10.1126\/science.152.3719.210"},{"key":"atypb22","doi-asserted-by":"publisher","DOI":"10.1128\/BR.11.2.115-145.1947"},{"key":"atypb23","doi-asserted-by":"publisher","DOI":"10.2307\/3001557"},{"key":"atypb24","doi-asserted-by":"crossref","first-page":"175","DOI":"10.1111\/j.2517-6161.1954.tb00159.x","volume":"16","author":"Fieller EC","year":"1940","journal-title":"J Roy Statist Soc"},{"key":"atypb25","doi-asserted-by":"publisher","DOI":"10.1126\/science.1281928"},{"key":"atypb26","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.87.4.1620"},{"key":"atypb27","doi-asserted-by":"publisher","DOI":"10.1007\/BF00570134"}],"container-title":["Human & Experimental Toxicology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/journals.sagepub.com\/doi\/pdf\/10.1177\/096032719601500103","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/journals.sagepub.com\/doi\/pdf\/10.1177\/096032719601500103","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2026,4,29]],"date-time":"2026-04-29T07:44:51Z","timestamp":1777448691000},"score":1,"resource":{"primary":{"URL":"https:\/\/journals.sagepub.com\/doi\/10.1177\/096032719601500103"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1996,1]]},"references-count":27,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1996,1]]}},"alternative-id":["10.1177\/096032719601500103"],"URL":"https:\/\/doi.org\/10.1177\/096032719601500103","relation":{},"ISSN":["0960-3271","1477-0903"],"issn-type":[{"value":"0960-3271","type":"print"},{"value":"1477-0903","type":"electronic"}],"subject":[],"published":{"date-parts":[[1996,1]]}}}