Regional accumulation of aluminium in the rat brain is affected by dietary vitamin E

Abubakar, M. G.; Taylor, Andrew; Ferns, Gordon A.

doi:10.1016/j.jtemb.2004.02.001

Cited by 34 publications

(24 citation statements)

References 37 publications

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“…injection of AlCl 3 for 60 days caused a significant and greater aluminium accumulation ( Fig. 1) in hippocampus and cortex, a finding that is consistent with previous studies [28,29]. Aluminium enters into the brain via the specific high affinity receptors for transferrin (TfR) expressed in the blood brain barrier [30] and accumulated in all the regions of rat brain, the maximum being in hippocampus, which is the site of memory and learning [31].…”

Section: Discussionsupporting

confidence: 88%

Neuroprotective Effect of Hesperidin on Aluminium Chloride Induced Alzheimer’s Disease in Wistar Rats

et al. 2015

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The present study was aimed to evaluate the protective effect of hesperidin (Hes) on aluminium chloride (AlCl3) induced neurobehavioral and pathological changes in Alzheimeric rats. Intraperitonial injection of AlCl3 (100 mg/kg body weight) for 60 days significantly elevated the levels of aluminium (Al), activity of acetylcholinesterase (AChE) and protein expressions of amyloid precursor protein (APP), β amyloid (Aβ 1-42), β and γ secretases as compared to control group in hippocampus and cortex of rat brain. Hes administration orally along with AlCl3 injection for 60 days, significantly revert the Al concentration, AChE activity and Aβ synthesis-related molecules in the studied brain regions. Our results showed that aluminum exposure was significantly reduced the spontaneous locomotor and exploratory activities in open field test and enhanced the learning and memory impairments in morris water maze test. The behavioral impairments caused by aluminum were significantly attenuated by Hes. The histopathological studies in the hippocampus and cortex of rat brain also supported that Hes (100 mg/kg) markedly reduced the toxicity of AlCl3 and preserved the normal histoarchitecture pattern of the hippocampus and cortex. From these results, it is concluded that hesperidin can reverse memory loss caused by aluminum intoxication through attenuating AChE activity and amyloidogenic pathway.

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Section: Discussionsupporting

confidence: 88%

Neuroprotective Effect of Hesperidin on Aluminium Chloride Induced Alzheimer’s Disease in Wistar Rats

et al. 2015

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“…However, all the aluminum-exposed animals showed insignificant reduction in cerebral catalase activity. This observation was in agreement with the earlier observation of aluminum-induced significant reduction in catalase activity in rat cerebrum [40]. The enhanced catalase activity in ethanol exposure may be due to up regulation of catalase mediated metabolism of ethanol [41] or an efficient decomposition of H 2 O 2 in the brain regions.…”

Section: Discussionsupporting

confidence: 93%

Augmentation of Aluminum-Induced Oxidative Stress in Rat Cerebrum by Presence of Pro-oxidant (Graded Doses of Ethanol) Exposure

2010

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Both aluminum and ethanol are pro-oxidants and neurotoxic. Considering the possibilities of co-exposure and sharing mechanisms of producing neurotoxicity, the present study was planned to identify the level of aluminum-induced oxidative stress in altered pro-oxidant (ethanol exposure) status of cerebrum. Male rats were coexposed to aluminum and ethanol for 4 weeks. After the exposure period, cerebral levels of protein, reduced glutathione (GSH), lipid peroxidation (TBARS) were measured. Activities of catalase, superoxide dismutase (SOD), glutathione reductase (GR) and glutathione perioxidase (GPx) of cerebrum were estimated. In most of the cases significant correlations were observed between the alterations and graded ethanol doses, suggesting a dose-dependency in pushing the oxidant equilibrium toward pro-oxidants. Aluminum is found to influence significantly all the studied parameters of oxidative stress. Likewise, ethanol also influenced these parameters significantly, except GR, while the interaction between ethanol and aluminum could significantly influence only the GSH content and GR activity of cerebrum. Present study demonstrate that coexposure of aluminum with pro-oxidant might favor development of aluminum-induced oxidative stress in cerebrum. This observation might be helpful in understanding of mechanism of neurodegenerative disorders and ameliorate them.

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“…The latter is the factor inducing oxidative stress in the brain, but this effect of Al 3+ can be completely compensated by injection of vitamin E [21]. It was found that vitamin E in food significantly decreased accumulation of Al 3+ in various brain structures of rats [22] and in the liver [23].…”

Section: Resultsmentioning

confidence: 99%

Effect of Vitamin E on the Content and Polypeptide Composition of Glial Fibrillary Acidic Protein from the Rat Brain under Conditions of Aluminum Chloride Intoxication

2005

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We studied the effects of isolated and combined chronic (21 days) introductions of aluminum chloride and vitamin E (α-tocopherol) on the polypeptide composition and content of glial fibrillary acidic protein (GFAP) in different brain structures of rats. Injections of AlCl 3 solution (12 mg/kg, i.p., daily) caused the appearance of low-molecular (47 to 38 kdalton) polypeptides and an increase in the content of GFAP in cytoskeletal fractions to 160 to 220%, as compared with the control. Introduction of vitamin E within the same interval provided significant normalization of the GFAP content in the brain of animals injected with AlCl 3 and to a considerable extent prevented the appearance of degraded polypeptides in the GFAP composition. We discuss the prospects of using vitamin E as an antioxidant for the correction of Al 3+ -induced pathological processes in the CNS.

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Regional accumulation of aluminium in the rat brain is affected by dietary vitamin E

Cited by 34 publications

References 37 publications

Neuroprotective Effect of Hesperidin on Aluminium Chloride Induced Alzheimer’s Disease in Wistar Rats

Neuroprotective Effect of Hesperidin on Aluminium Chloride Induced Alzheimer’s Disease in Wistar Rats

Augmentation of Aluminum-Induced Oxidative Stress in Rat Cerebrum by Presence of Pro-oxidant (Graded Doses of Ethanol) Exposure

Effect of Vitamin E on the Content and Polypeptide Composition of Glial Fibrillary Acidic Protein from the Rat Brain under Conditions of Aluminum Chloride Intoxication

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