The authors are studying the molecular details of the process that begins with hepatic metabolism of halogenated inhalation anesthetics and ends with hepatic necrosis. In previous studies they have shown that the halothane-free radical produced by UV-irradiation is identical to that produced during reductive metabolism of halothane by hepatic cytochrome P-450. In the present study, the authors have examined a mechanism by which free radicals may propagate damage in the endoplasmic reticulum of liver cells. The 1-chloro-2,2,2-trifluoroethyl free radical produced by UV-irradiation of halothane can abstract a hydrogen radical from arachidonic acid to yield 2-chloro-1,1,1-trifluoroethane and an arachidonic acid-free radical. The arachidonic acid-free radical reacts with molecular oxygen to form 5− and 15-hydroperoxyeicosatetraenoic acid. There is considerable evidence that the peroxidation process that we studied in the model system will be similar when the arachidonic acid is an acyl chain on a membrane phospholipid and the free radicals are generated metabolically. The authors suggest that these hydroperoxides may be toxic by acting as intermediates in the pathway of leukotriene production as well as by direct oxidation of membrane components.