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Abstract
1. 2-Ethylhexanol was efficiently absorbed following oral administration to rats.
14C associated with 2-ethyl[1-14C]hexanol was rapidly excreted in respiratory CO2
(6-7%), faeces (8-9%) and urine (80-82%), with essentially complete elimination by
28 h after administration. 2. The amount of label recovered in 14CO2 matched the amount
of unlabelled 2-heptanone plus 4-heptanone recovered from urine, suggesting that both
types of metabolite may have been derived form the major urinary metabolite, 2-ethylhexanoic
acid, by decarboxylation following partial beta-oxidation. The 14CO2 appeared not
to be derived from acetate (urinary acetic acid and liver and brain cholesterol were
not labelled) or by reductive decarboxylation (heptane was not present.) 3. Other
identified metabolites were 2-ethyl-5-hydroxyhexanoic acid, 2-ethyl-5-ketohexanoic
acid, and 2-ethyl-1,6-hexanedioic acid. Only about 3% of the ethylhexanol was excreted
unchanged. 4. Ethylhexanol was a competitive inhibitor of yeast alcohol dehydrogenase,
but a good substrate for horse alcohol dehydrogenase. 5. Other relationships between
metabolism and toxicity of 2-ethylhexanol are discussed.