Methods: Male 30-day-old Wistar rats received a single subcutaneous Phe injection (5.2 μmol/g) and/or p-chlorophenylalanine (p-Cl-Phe; 0.9 μmol/g), an inhibitor of phenylalanine hydroxilase. Control group received saline solution at the same volume. One hour after Phe administration, cerebral cortex was isolated and the levels of the cytokines interleukine-1B (IL-1B), interleukine 10 (IL-10) and α-tumoral necrosis factor (TNFα) were evaluated. Results: IL-1B and IL-10 levels were increased by the simultaneous administration of Phe and p-Cl-Phe, but not by isolated administration. On the other hand, TNFα levels increased in animals receiving Phe, p-Cl-Phe or Phe plus p-Cl-Phe, as compared to control group. Conclusion: Taken together, these data suggest that Phe administration alters cytokine homeostasis in brain of young rats. Our results may help to explain, at least in part, the characteristic brain impairment observed in PKU patients. Financial Support: L'Oreal/ABC/UNESCO, PIBIC/UNESC and CNPq. Background: Glutathione (GSH) is an important antioxidant that eliminates reactive species and acts as cofactor for many antioxidant enzymes. Several studies have reported the involvement of oxidative stress in PKU patients and changes in GSH/GSSG ratio (an important index of oxidative stress) were found in tissues from a hyperphenylalaninemia (HPA) animal model. Objectives: The activity of some enzymes involved in GSH metabolism was evaluated in brain of rats subjected to a chemically-induced HPA. Material and methods: Six-day-old Wistar rats received daily injections of α-methyl-phenylalanine (1,6 μmol/g), phenylalanine hydroxylase inhibitor, and Phe (2,1 μmol/g) for 7 days. Controls received saline instead. Animals were killed and the brain removed and homogenated to measure the activity of glucose-6-phosphate dehydrogenase (G6PD), glutathione peroxidase (GPx), glutathione reductase (GR), glutathione-S-transferase (GST) and glutamylcysteine ligase (GCL).