Aluminum exposure through the diet: Metal levels in AβPP transgenic mice, a model for Alzheimer's disease

Gómez, Mercedes; Esparza, José L.; Cabré, María; García, Tánia; Domingo, José L.

doi:10.1016/j.tox.2008.05.004

Cited by 53 publications

(92 citation statements)

References 52 publications

(88 reference statements)

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“…Regular chow was supplemented with 1 mg of Al per gram of chow (Harlan Ibérica, Barcelona, Spain) (Gómez et al, 2008). Melatonin was also purchased from Sigma Chemical.…”

Section: Chemicals Animals and Treatmentmentioning

confidence: 99%

“…It is a progressive neurodegenerative disorder that gradually deprives the patient of cognitive function. AD is mainly characterized by the presence of neuritic plaques and neurofibrillary tangles in hippocampus and neocortex of the brain (Yokel and Florence, 2006;Shcherbatykh and Carpenter, 2007;Gómez et al 2008). The neuropathological characteristics of AD include cortical and subcortical atrophy, formation of intraneuronal neurofibrillary tangles, deposition of amyloid beta peptide (Ab) in neuritic plaques or senile plaques, and formation of neuropil threads, loss of synaptic function, oxidative stress and apoptosis, leading to neuronal loss (Kaneko et al, 2004, Gupta et al, 2005, Hirata-Fukae et al, 2008.…”

Section: Introductionmentioning

confidence: 99%

“…This mouse is currently considered as an experimental model of AD (Chapman et al, 1999;Pratico et al, 2002;Rodrigo et al, 2004;Maynard et al, 2006;López-Toledano andShelanski, 2007, Duyckaerts et al, 2008). Only results of a few studies concerning Al effects in these animals have been reported (Pratico et al, 2002;Drago et al, 2008;Gómez et al, 2008;Ribes et al, 2008). In relation to it, Pratico et al (2002) studied in Tg2576 mice the effects of dietary Al administration (2 mg of Al/kg of diet).…”

Section: Introductionmentioning

confidence: 99%

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Oxidative stress status and RNA expression in hippocampus of an animal model of Alzheimer's disease after chronic exposure to aluminum

et al. 2009

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It is well established that aluminum (Al) is a neurotoxic agent that induces the production of free radicals in brain. Accumulation of free radicals may cause degenerative events of aging such as Alzheimer's disease. On the other hand, melatonin (Mel) is a known antioxidant, which can directly act as free radical scavenger, or indirectly by inducing the expression of some genes linked to the antioxidant defense. In this study, AbetaPP female transgenic (Tg2576) (Tg) and wild-type mice (5 months of age) were fed with Al lactate supplemented in the diet (1 mg Al/g diet). Simultaneously, animals received oral Mel (10 mg/kg) dissolved in tap water until the end of the study at 11 months of age. Four treatment groups were included for both Tg and wild-type mice: control, Al only, Mel only, and Al+Mel. At the end of the period of treatment, hippocampus was removed and processed to examine the following oxidative stress markers: reduced glutathione (GSH), oxidized glutathione (GSSG), superoxide dismutase (SOD), glutathione reductase (GR), glutathione peroxidase (GPx), catalase (CAT), and thiobarbituric acid reactive substances (TBARS). Moreover, the gene expression of Cu-ZnSOD, GR, and CAT was evaluated by real-time RT-PCR. Aluminum concentration in hippocampus was also determined. The biochemical changes observed in this tissue suggest that Al acts as a pro-oxidant agent. Melatonin exerts an antioxidant action by increasing the mRNA levels of the antioxidant enzymes SOD, CAT, and GR evaluated in presence of Al and Mel, with independence of the animal model.

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“…Regular chow was supplemented with 1 mg of Al per gram of chow (Harlan Ibérica, Barcelona, Spain) (Gómez et al, 2008). Melatonin was also purchased from Sigma Chemical.…”

Section: Chemicals Animals and Treatmentmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Oxidative stress status and RNA expression in hippocampus of an animal model of Alzheimer's disease after chronic exposure to aluminum

et al. 2009

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“…Al is believed to be a cofactor or an aggravating factor in the pathologies of both AD and PD, although there are still many contradictory data among epidemiological studies, analytical measurements, and clinical examinations. [1][2][3] The causative role of AD was confirmed to be related to familial autosomal problems, such as the beta amyloid (Aβ) pathway, tau presenilins and ApoE. 4 Al was identified to have a special effect in enhancing Aβ toxicity.…”

Section: Introductionmentioning

confidence: 99%

Electrochemical and Spectrometric Studies of Double-Strand Calf Thymus Gland DNA Denatured by Al(III) at Neutral pH

et al. 2009

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The interaction between double-strand calf thymus gland DNA (ds-DNA) and Al(III) was studied by using differential pulse voltammetry (DPV) at a hanging mercury drop electrode (HMDE), Raman spectrometry and circular dichroism (CD) spectra. It was shown that at neutral pH ds-DNA did not produce any cathodic peak at the HMDE in the potential window from -550 to -2000 mV vs. SCE. However, in the presence of Al(III), a cathodic peak was generated at about -1660 mV, which is ascribed to a reduction of adenine and cytosine residues of single denatured DNA (sd-DNA). It was concluded that ds-DNA was completely denatured to sd-DNA by Al(III) at a neutral pH. The apparent denaturing kinetic velocity constants of ds-DNA by Al(III) were derived from linear increases of the cathodic peak currents with time.3 ≥ 2 × 10 -26 , the precipitation of Al(OH)3 was observed and identified by the Raman spectrum, and inductively coupled plasma atomic emission spectrometry (ICP-AES). CD spectra showed that the B-type of structure conformations of ds-DNA and related sd-DNA did not change with the increment of Al(III) from 5.0 × 10 -7 to 1.0 10 -5 M, but the corresponding absorption strengths increased. The related physiological significances and possible applications of the observations were considered.

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“…Industrialization has led to a higher frequency of acid rain which in Aluminum toxicity has been extensively studied for its implication in neurodegenerative diseases such as Alzheimer's disease (AD) and multiple sclerosis (MS). The brain is an important Al accumulating organ, yet Al can also concentrate more severely in other tissues of the human body (Figure 4) (Gomez et al, 2008;Rondeau et al, 2008). Nonetheless, aluminum salts such as aluminum hydroxides and aluminum phosphates are routinely used in medical practices as the only licensed adjuvants in vaccines.…”

Section: Sourcementioning

confidence: 99%

The Molecular Connection Between Aluminum Toxicity, Anemia, Inflammation and Obesity: Therapeutic Cues

Bignucolo¹,

Lemire²,

Auger³

et al. 2012

Anemia

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Aluminum exposure through the diet: Metal levels in AβPP transgenic mice, a model for Alzheimer's disease

Cited by 53 publications

References 52 publications

Oxidative stress status and RNA expression in hippocampus of an animal model of Alzheimer's disease after chronic exposure to aluminum

Oxidative stress status and RNA expression in hippocampus of an animal model of Alzheimer's disease after chronic exposure to aluminum

Electrochemical and Spectrometric Studies of Double-Strand Calf Thymus Gland DNA Denatured by Al(III) at Neutral pH

The Molecular Connection Between Aluminum Toxicity, Anemia, Inflammation and Obesity: Therapeutic Cues

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