SummaryAldehyde oxidase (AO) is a molybdo-avo enzyme expressed predominantly in the liver, lung, and kidney. AO plays a major role in oxidation of aldehydes, as well as oxidation of various Nheterocyclic compounds of pharmacological and toxicological importance including antiviral (famciclovir), antimalarial (quinine), antitumour (methotrexate), and nicotine. The aim of this study was to investigate cytosolic aldehyde oxidase activity in human liver. Cytosolic AO was characterised using both the metabolism of N-[(2-dimethylamino)ethyl] acridine-4-carboxamide (DACA) and benzaldehyde to form DACA-9(10H)-acridone (quanti ed by HPLC with uorescence detection) and benzoic acid (quanti ed spectrophotometrically ). Thirteen livers (10 female, 3 male) were examined. The intrinsic clearance (Vmax/Km) of DACA varied 18-fold (0.03-0.50 ml/min/mg). Vmax ranged from 0.20 -3.10 nmol/ min/mg, and Km ranged from 3.5 -14.2 ¹M. In the same specimens, the intrinsic clearance for benzaldehyde varied 5-fold (0.40-1.8 ml/min/mg). Vmax ranged from 3.60 -12.6 nmol/min/mg and Km ranged from 3.6 -14.6 ¹M. Furthermore, there were no differences in AO activity between male and female human livers, nor was there any relationship to age of donor (range 29 -73 years), smoking status, or disease status. In conclusion, our results showed that there are variations in AO activity in human liver. These variations in aldehyde oxidase activity might re ect individual variations or they might be due to AO stability during processing and storage.

This study showed that short-term (40-80 min) nitrous oxide anaesthesia did not affect cobalamin levels but reduced serum folate levels in this elderly population. Although this reduction was clinically irrelevant, some patients with pre-existing asymptomatic folate deficiency developed nitrous oxide-induced folate deficiency.

The availability of safer drugs should result in a complete ban of these dangerous compounds.

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