Degradation of Salicylate by Aspergillus niger

Abstract

SALICYLATE continues to be a leading cause of accidental poisoning in the United States; in 1964 there were more than 16,000 cases of accidental aspirin ingestion among all age groups, accounting for 25.8 per cent of all accidental poisonings reported¹. Existing methods for the treatment of salicylate poisoning are aimed at alkalinization of the urine and extrarenal removal of the drug^2,3. The natural elimination of salicylate in man is a slow process. The average half-life of a single 1 g dose of aspirin is reported to be 6 h (ref. 4), and high doses have given half-life values up to 19 h (ref. 5). Administration of salicylate labelled with carbon-14 to man⁶ has given the following metabolites (here reported as average mean values): free salicylate 61 per cent; salicylic phenolic glucuronide 22 per cent; salicyluric acid 8 per cent; salicylic acyl glucuronide 5 per cent; and gentisic acid 1 per cent. The conjugates of salicylic acid are less diffusible across cell membranes and thus have given higher clearances⁷. Furthermore, the excretion of salicyluric acid after administration of acetylsalicylate or salicylate is limited by the ability to conjugate salicylate with glycine rather than the excretion capacity of the kidneys⁸.