Liver and heart toxicity due to 90-day oral exposure of ICR mice to N,N-dimethylformamide

Abstract

N,N-dimethylformamide (DMF) is a colorless liquid with a faint amine odor, which is widely used in the world. DMF exposure may induce adverse effects on liver, but few studies showed damage to heart after exposure to DMF. In the present study, DMF was administered to ICR mice with the doses of 0.32, 0.63 and 1.26 g/kg of body weight by gavage for 90 days. The increase in the relative liver weight is accompanied with the presence of the centrilobular hepatocellular hypertrophy as well as increased serum levels of aspartate transaminase (AST) and alanine transaminase (ALT). An increase of malondialdehyde (MDA) level was shown in liver homogenate, while superoxide dismutase (SOD) and glutathione (GSH) activities decreased. Heart damage was also shown in mice exposed to DMF for 90 days, although pathological examination showed only slight inflammatory cell infiltration. Increased levels of serum lactate dehydrogenase (LDH), isoenzymes of creatine kinase (CK-MB) and cardiac troponin I (cTnI) were shown. Increased level of MDA was also shown in heart homogenate, in contrast with the decreased activity of SOD. These data suggested that the administration of DMF could induce liver and heart injuries and oxidative stress was involved in the toxic effects.