New sources of dioxins and increased dioxin concentrations in the environment, coupled with their increased bioavailability along the food chain and accumulation in adipose tissues, contribute to various adverse long-term biological effects. The purpose of the study was to determine whether tocopherol protects the CNS by decreasing the pro-inflammatory influence of free radicals generated by TCDD; whether acetylsalicylic acid inhibits the production of inflammatory mediators; and whether the combined administration of tocopherol and acetylsalicylic acid to TCDD-exposed rats has a potential CNS-protective effect. The study included 117 rats divided into 8 groups: 75 female and 12 male Buffalo rats aged 8–10 weeks, weighing 140–160g; as well as 30 female rats aged 6 weeks and weighing 120g, which were the offspring of females from each study group. In the experiment, the following substances were used: 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), dosed at 5μg/kg BW and 12.5μg/kg BW, diluted in a 1% DMSO solution at the concentration of 1μg/ml; α-tocopherol acetate, dosed at 30mg/kg BW, in 0.2ml of oil solution; and acetylsalicylic acid, 50mg/kg BW, suspended in 0.5ml of starch solution, administered orally using a feeding tube. Pleurisy was induced by an injection of 0.15ml of 1% carrageenin solution. The use of tocopherol reduces the adverse effects of the inflammatory reaction induced by TCDD. Administering tocopherol improves protein metabolism by reducing protein catabolism, and raises γ-globulin fraction levels. Combined acetylsalicylic acid and tocopherol suppress catabolic processes accompanying inflammation.