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.

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.

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).