The effects of methionine (Met) on the toxicities of methylmercury (MeHg) and atrazine in male Wistar rats were investigated. Three levels of dietary Met, three levels of MeHg by gavage, and two levels of dietary atrazine were used. A two-choice form light discrimination test was used to investigate behavioral effects of the treatments. Samples of blood, liver, kidney, and brain were collected for glutathione peroxidase (GSH-Px), glutathione reductase (GSH-Rd), glutathione-S-transferase (GSH-S-trans), total glutathione (GSH), prostaglandin (PG), and mercury analyses. Excess dietary Met had a protective effect on MeHg and atrazine toxicities in rats, using weight gain as the index of toxicity. Liver weight in response to the toxicants was increased in the groups of rats which were fed the lower Met levels but there was no change in those fed the highest level of Met. The highest Met level caused a lower increase in kidney weight in rats treated with MeHg. The lowest Met level caused greater mercury uptake in the organs. Atrazine caused a significant increase in mercury excretion in urine after three weeks of exposure but not at the end of the experiment, suggesting adaption. In whole blood but not in liver, GSH-Px activity declined as mercury concentration increased. Atrazine lowered liver GSH-S-trans activity. Increases in MeHg dose caused a decrease in GSH-S-trans activity in the rats fed the lowest Met level but increased it with the other diets. Treatments with MeHg caused increased synthesis of PG by platelets. Dietary Met had no effect on liver GSH but increased oxidized and total GSH in blood. Atrazine increased urinary mercapturic acid excretion. Despite clinical and biochemical effects of the treatments, the behavioral tests were negative.