Adult male Swiss strain albino mice (Mus musculus) were administered orally sodium fluoride (NaF, 10 mg/kg bw), aluminium chloride (AlCl3, 200 mg/kg bw), or both together for a period of 30 days to study the induction of free radical toxicity in their liver. The effects of withdrawal of treatment (30 days) as well as the beneficial effects, if any, of vitamin C (15 mg/animal/day) or vitamin E (2 mg/animal/day) administered alone were also investigated. Fluoride, alone and in combination with aluminium, significantly (P<0.001) impaired the production of free radical scavengers, superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), glutathione (GSH), and total ascorbic acid (TAA), thereby increasing hepatic lipid peroxidation and thus making the tissue more susceptible to injury. Cessation of the NaF and AlCl3 treatments for the next 30 days brought about measurable recovery of most of these parameters in the liver as compared to the treated group of mice. However, pronounced or even complete recovery occurred in all parameters (P<0.001) by administration of ascorbic acid (vitamin C) or vitamin E during the 30-day recovery period. The results show that mice liver function can recover after fluoride and aluminium induced intoxication by the mitigating effects of vitamins C and E.