Abstract
BackgroundHigher 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.MethodsPostnatal 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.ResultsAluminum 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.ConclusionAluminum overload increases oxidative stress (H2O2) in the hippocampus, diencephalon, cerebellum, and brain stem in neonatal rats.
Highlights
Higher aluminum (Al) content in infant formula and its effects on neonatal brain development are a cause for concern
The brain stem weights were significantly lower in the high Al (HA) group than in the control group (0.19 ± 0.05 g v.s. 0.24 ± 0.06 g; p < 0.05)
The average cerebellar weight to body weight ratio was significantly lower in the HA group than in the control group (0.48 ± 0.18% v.s. 0.71 ± 0.24%; p < 0.05), while the average olfactory bulb weight to body weight ratio was significantly higher in the HA group than in the low Al (LA) group (0.28 ± 0.15% v.s. 0.16 ± 0.05%; p < 0.05) (Table 2)
Summary
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. Brain tissues are highly susceptible to oxidative damage, probably because of high oxygen consumption rate (20%), the presence of abundant polyunsaturated fatty acids in cell membranes, high iron (Fe) content, and low anti-oxidative enzyme activities [2]. It can bind to negatively charged brain phospholipids, which contain polyunsaturated fatty acids and are attacked by reactive oxygen species (ROS) such as O2 ̇-, H2O2, OH, and OH- [3]. Aluminum can stimulate iron-initiated lipid peroxidation in the Fenton reaction, which causes ROS production and Fe3+ formation. Superoxide (O2 ̇-) is neutralized by Al3+ to form an Al-O2 ̇- complex, which increases the oxidative capacity of O2 ̇- [4]
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