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

BACKGROUND: Higher aluminum (Al) content in infant formula and its effects on neonatal brain development are a cause for concern. This study aimed to evaluate the distribution and concentration of Al in neonatal rat brain following Al treatment, and oxidative stress in brain tissues induced by Al overload. METHODS: 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. RESULTS: 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. CONCLUSION: Aluminum overload increases oxidative stress (H2O2) in the hippocampus, diencephalon, cerebellum, and brain stem in neonatal rats.

Aluminum alters NMDA receptor 1A and 2A/B expression on neonatal hippocampal neurons in rats.

BACKGROUND: High aluminum (Al) content in certain infant formula raises the concern of possible Al toxicity on brain development of neonates during their vulnerable period of growing. Results of in vivo study showed that Al content of brain tissues reached to 74 µM when oral intake up to 1110 µM, 10 times of that in the hi-Al infant formula. METHODS: Utilizing a cultured neuron cells in vitro model, we have assessed Al influence on neuronal specific gene expression alteration by immunoblot and immunohistochemistry and neural proliferation rate changes by MTT assay. RESULTS: Microscopic images showed that the neurite outgrowth of hippocampal neurons increased along with the Al dosages (37, 74 µM Al (AlCl3)). MTT results also indicated that Al increased neural cell viability. On the other hand, the immunocytochemistry staining suggested that the protein expressions of NMDAR 1A and NMDAR 2A/B decreased with the Al dosages (p < 0.05). CONCLUSION: Treated hippocampal neurons with 37 and 74 µM of Al for 14 days increased neural cell viability, but hampered NMDAR 1A and NMDAR 2A/B expressions. It was suggested that Al exposure might alter the development of hippocampal neurons in neonatal rats.

Effects of peritoneal aluminum overload on polyamines and nitric oxide contents of testes and epididymis in the mice.

Polyamines are involved in cellular growth, differentiation and regulation of oxidative stress. The present investigation was to determine the effect of aluminum (Al) toxicity on the nitric oxide products (NO(x)) and metabolism of polyamines in mouse testes and epididymis. Aluminum chloride, AlCl(3,) was administered intraperitoneally to CD-1 adult male mice at dosages of 0, 7 or 35mg Al/kg body weight/day for 14 days (C, LAL and HAL groups). Results obtained show that the weights of epididymis in HAL animals are significantly decreased due to Al administration. Al treatment significantly induced higher Al concentrations in serum, testis and epididymis tissue. In addition, the serum and testicular and epididymal NO(x) production in HAL and testicular NO(x) in LAH groups were increased remarkably compared to the control animals. On the contrary, the contents of putrescine and spermine in testis were significantly lower than the values of controls and LAL groups. The epididymal spermine levels of HAL animal also decreased significantly. It is suggested that the polyamine biosynthesis in the mouse testis and epididymis can be affected by Al, which is associated with the NO(x) production in the male reproductive toxicity.