Toxicology, 43 (1987) 231--238 Elsevier Scientific Publishers Ireland Ltd. REVIEW PAPER DIMETHYLFORMAMIDE (DMF) HEPATOTOXICITY* VERONIQUE SCAILTEUR** and R.R. LAUWERYS Industrial Toxicology Unit, Catholic University of Louvain, Clos Chapelle aux Champs 3054, B-1200 Brussels (Belgium) (Received June 13th, 1986) (Accepted September 12th, 1986) SUMMARY Scattered case reports of accidental exposure and a few epidemiological studies have indicated that the liver is the main target organ following acute and chronic exposure to dimethylformamide (DMF). This has been con- firmed in several animal species. In humans, ethanol intolerance is one of the earliest manifestations of (excessive) exposure to DMF, followed at higher exposure levels by various complaints (nausea, vomiting, abdominal pain) and the release of liver cytolytic enzymes in the plasma. The metabolic path- way of DMF has been recently clarified, but the primary cellular lesion responsible for its hepatotoxicity is still unknown. Key words: Dimethylformamide; Solvent; Hepatotoxicity INTRODUCTION Dimethylformamide (DMF) is widely used as an organic solvent in the laboratories and in the chemical industry (e.g. in the production of acrylic *Presented at the symposium on "Biological Properties and Toxicity of Formamides", held at the Aston University, Birmingham, U.K., in May 1986. **Present address: Procter and Gamble European Technical Center, Temselaan, 100, B-1820 Strombeek-Bever, Belgium. Abbreviations: AP, alkaline phosphatase; 7-GT, gamma-glutamyl transferase; GDH, gluta- mate dehydrogenase; GOT, glutamate oxalate transaminase; GPT, glutamate pyruvate transaminase; i.p., intraperitoneal; OCT, ornithine carbamyl transferase; MDA, malon- dialdehyde; s.c., subcutaneous; SDH, sorbitol dehydrogenase. o3oo-483x/87/$o3.5o © 1987 Elsevier Scientific Publishers Ireland Ltd. Printed and Published in Ireland 231