Fatty acid changes in rat brain ethanolamine phosphoglycerides during and following chronic exposure to trichloroethylene.

Rats were exposed by continuous inhalation to a moderate level of trichloroethylene (1720 mg/m3). The fatty acid pattern of brain ethanolamine phosphoglycerides was examined during exposure and after an additional exposure-free period. Alterations in the fatty acid pattern were noted after 30 days of exposure. An increased ratio of linoleic acid-derived (n-6) to linolenic acid-derived (n-3) fatty acids was observed in the cerebral cortex, the hippocampus, and the brain stem. Of the major fatty acids, arachidonic acid (20:4(n-6)) was increased in the cerebral cortex and the brain stem, while docosahexenoic acid (22:6(n-3)) was decreased in the cerebral cortex and the hippocampus. A further change in these fatty acids was observed in the cerebral cortex following a longer exposure period of 90 days. The 22-carbon linoleic acid-derived fatty acids were also increased after 90 days of exposure. These findings imply that trichloroethylene affects the metabolism of ethanolamine phosphoglyceride fatty acids in the rat brain by inhibiting desaturation of the linolenic acid family and by increasing desaturation of the linoleic acid family. The effect of trichloroethylene was partially reversible, since a postexposure solvent-free period revealed a rapid partial normalization of 22:6(n-3), which is the most important fatty acid of the linolenic acid family in the rat brain. However, the precursor of this fatty acid, 22:5(n-3), was decreased during the first 10 exposure-free days. This suggests that desaturation over the first steps was still impaired. A complete normalization of the fatty acid pattern was not observed during the 30-day solvent-free period. The decreased number of double bonds and shorter chain lengths detected after solvent exposure is consistent with the idea of a compensatory remodeling of membrane lipid composition based on membrane stability with regard to phase preference.