The anti-peroxidant effect of intravenous magnesium was evaluated in 50 patients with acute aluminium phosphide poisoning. The patients were divided into two groups, one who received magnesium sulphate therapy (Group I) and the other who did not (Group II). The clinical and biochemical parameters in both groups were comparable. Finding of increased mean malonyl-di-aldehyde (MDA) levels in group I (3.18 +/- 0.93 micromol/L) and group II (3.15 +/- 0.78 mmol/L) combined with low blood levels of reduced glutathione (18.5 +/- 1.6 mg/dl in group I) and (17.8 +/- 1.4 mg/dl in group II) indicated oxidative stress leading to accelerated lipid peroxidation in the early phase (0-6 h) of AlP poisoning. A significant fall in MDA levels was observed after 2 h in the magnesium treated group (group I) compared to the non-treated group (group II) and levels became normal between 48-72 h. Similarly reduced glutathione started recovering between 12-24 h which became significant after 24 h and full recovery took place between 48-72 h in the magnesium treated group (group I). Both these parameters suggested an anti-peroxidant effect of magnesium. There was also a slight fall in MDA levels and a rise in reduced glutathione in the non-treated group II patients. This could be due to elimination of phosphine (PH3). We hypothesize that oxidative stress in AlP poisoning buffered the magnesium leading to a transient fall in magnesium and magnesium dependent GSH, resulting in increased susceptibility of oxygen free radical injury and accelerated lipid peroxidation. The fall in MDA and slower rise in GSH in group I than in group II suggested magnesium combated free radical stress slowly and independent of elimination of phosphine. This hypothesis was further strengthened by similar observations when both these parameters were compared in survivors in both groups. Mortality was higher in group II than in group I (44 per cent vs 20 per cent) and was probably related directly to oxidative stress.