One hundred and forty rats were treated with ovex ( p-chlorophenyl p-chlorobenzenesulfonate) 100 mg/kg orally, paired with an equal number of controls, grouped (20 treated and 20 control) and designated as 12, 24, 48, 72, 96, 240, and 360 hr. Ten treated and ten control were given a lethal dose of parathion (100 mg/kg, oral) at the designated times after ovex and the length of survival recorded. Similar groups were killed at the designated times and the liver wt/body wt ratio, and α-naphthyl acetate hydrolyzing activity of 9000X g liver supernate determined. Significant increases in liver wt/body wt ratio and α-naphthyl acetate hydrolyzing activity were observed. When the above increases in liver size and enzyme activity were combined and expressed as a percentage, peak activity was seen at 72 hr (181%) and was present up to 240 hr (129%). Ovex (100 mg/kg oral) pretreatment appeared to provide more protection against parathion than paraoxon toxicity. It increased the rate of parathion metabolism by whole liver homogenates but had only a marginal effect on the rate of metabolism of paraoxon ( p < 0.10). Ovex treatment reduced the liver organophosphate content of parathion but not paraoxon-exposed rats. An effect of ovex on plasma and brain organophosphate concentrations was not demonstrated.