Aluminum overload increases oxidative stress in four functional brain areas of neonatal rats

Postnatal day 3 (PND 3) rat pups (n =46) received intraperitoneal injection of aluminum chloride (AlCl3), at dosages of 0, 7, and 35 mg/kg body wt (control, low Al (LA), and high Al (HA), respectively), over 14 d.Aluminum concentrations were significantly higher in the hippocampus (751.0 ±？225.8 ng/g v.s. 294.9？± 180.8 ng/g; p < 0.05), diencephalon (79.6？± 20.7 ng/g v.s. 20.4？±？9.6 ng/g; p？<？0.05), and cerebellum (144.8？± 36.2 ng/g v.s. 83.1 ± 15.2 ng/g; p？<？0.05) in the HA group compared to the control. The hippocampus, diencephalon, cerebellum, and brain stem of HA animals displayed significantly higher levels of lipid peroxidative products (TBARS) than the same regions in the controls. However, the average superoxide dismutase (SOD) activities in the cerebral cortex, hippocampus, cerebellum, and brain stem were lower in the HA group compared to the control. The HA animals demonstrated increased catalase activity in the diencephalon, and increased glutathione peroxidase (GPx) activity in the cerebral cortex, hippocampus, cerebellum, and brain stem, compared to controls.Aluminum overload increases oxidative stress (H2O2) in the hippocampus, diencephalon, cerebellum, and brain stem in neonatal rats.