Lipid peroxidation in vivo monitored as ethane exhalation and malondialdehyde excretion in urine after oral administration of chloroform.

In vivo lipid peroxidation was studied in phenobarbital pretreated rats exposed for chloroform. Lipid peroxidation was monitored as ethane exhalation or malondialdehyde (MDA) excretion in urine. A single oral dose of chloroform (0.7 ml/kg b.wt.) showed a marked increase in ethane exhalation in animals starved for 48 hours prior to chloroform treatment. This increase became evident after a lag-period of about 100 min. Pretreatment with diethylmaleate (1 ml/kg b.wt.) 1 hour prior to chloroform treatment gave a similar result. MDA excretion in urine from non-starved animals, exposed to chloroform, markedly increased after 4 hours and after 24 hours 115 nmol/kg had been excreted. In animals starved for 48 hours prior to chloroform treatment about 270 nmol/kg excreted within 24 hours. Small molecular weight thiols were measured in liver, kidneys and lungs. Chloroform decreased the thiol content of the liver by 43.2% within 100 min. while the concentration in the kidneys and the lungs were less affected. It is suggested that chloroform may act as a potent inducer of lipid peroxidation in vivo. The synergistic effects of the pretreatments and the lag phase indicate that glutathione depletion in the liver was an essential factor in this response.