{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T23:17:35Z","timestamp":1792192655394,"version":"4.4.0"},"reference-count":34,"publisher":"SAGE Publications","issue":"3","license":[{"start":{"date-parts":[[1990,5,1]],"date-time":"1990-05-01T00:00:00Z","timestamp":641520000000},"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":[[1990,5]]},"abstract":"1 The urinary recovery of metabolites of aspirin (ASA) was studied in 45 volunteers who took a therapeutic dose (600 mg) of ASA by mouth and in 37 patients who took ASA in overdose.<\/jats:p>\n 2 The main metabolite recovered from the volunteers was the glycine conjugate, salicyluric acid (SUA), which accounted for 75.01 \u00b1 1.19% of total urinary metabolites, whereas salicylic acid (SA) accounted for 8.82 \u00b1 0.56%. Recovery of SUA was negatively correlated with that of SA (r = -0.8625, P < 0.001).<\/jats:p>\n 3 In 24 patients with admission plasma salicylate concentrations of 240-360 mg 1-1, SUA accounted for 46.66 \u00b1 3.22% and SA for 31.88 \u00b1 4.02%.<\/jats:p>\n 4 In 13 patients with admission plasma salicylate concentrations of 715-870 mg 1-1, SUA accounted for 21.57 \u00b1 3.65% and SA for 64.72 \u00b1 4.82%.<\/jats:p>\n 5 Reduced excretion of salicylate as SUA was also accompanied by increased elimination as gentisic acid and salicylic acid phenolic glucuronide indicating that the unsaturated processes that lead to the formation of these metabolites contribute significantly (22-23%) to the inactivation of large doses of salicylate.<\/jats:p>\n 6 While the Michalis-Menten kinetics of ASA have been well demonstrated at lower doses, our findings illustrate the progressive saturation of SUA formation under conditions of increasing ASA load to toxic amounts and raise issues about the in-vivo glycine pool when ASA is taken in overdose.<\/jats:p>","DOI":"10.1177\/096032719000900302","type":"journal-article","created":{"date-parts":[[2008,12,24]],"date-time":"2008-12-24T01:08:04Z","timestamp":1230080884000},"page":"131-136","source":"Crossref","is-referenced-by-count":24,"title":["Metabolism of Aspirin after Therapeutic and Toxic Doses"],"prefix":"10.1177","volume":"9","author":[{"given":"D.K.","family":"Patel","sequence":"first","affiliation":[{"name":"Medicinal Biochemistry Department, Burroughs Wellcome Co., 3030 Cornwallis Road, Research Triangle Park, North Carolina 27709, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A.","family":"Hesse","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Ghana Medical School, PO Box 4226, Accra, Ghana"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A.","family":"Ogunbona","sequence":"additional","affiliation":[{"name":"Department of Pharmaceutical 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