Acetylcholinesterase activation and enhanced lipid peroxidation after long-term exposure to low levels of aluminum on different mouse brain regions

Kaizer, Rosilene Rodrigues; Junior, Marcos Corrêa; Spanevello, Rosélia Maria; Morsch, Vera Maria; Mazzanti, Cíntia M.; Gonçalves, Jamile Fabbrin; Schetinger, Maria Rosa Chitolina

doi:10.1016/j.jinorgbio.2005.06.015

Cited by 137 publications

(93 citation statements)

References 35 publications

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“…The present results are also in parallel with those previously recorded a significant increase in ACHE content in rats treated with AlCl 3 (50 mg/kg) daily for three months [52]. It is also reported that ACHE content in different brain regions increased after administration of AlCl 3 [53]. The elevation in ACHE content may be attributed to the direct neurotoxic effect of Al or to the disarrangement of the cell membrane phospholipids caused by the associated increase in lipid peroxidation [54].…”

Section: Discussionsupporting

confidence: 91%

Comparative Study on the Influence of Epigallocatechin-3-gallat e and/ or Coenzyme Q10 against Alzheimer's disease Induced by Aluminium in Normally-Fed and Protein Malnourished Rats

Ali¹,

Ahmed²

2016

J Alzheimers Dis Parkinsonism

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Background: Alzheimer's disease (AD) is a neurodegenerative disorder greatly influenced by oxidative stress and mitochondrial dysfunction which may lead to deposition of β-amyloid (Aβ) peptides. Protein malnutrition increases oxidative damage in cortex, hippocampus and cerebellum. Epigallocatechin-3-gallate (EGCG) has health-promoting effects in CNS, while Coenzyme Q10 (CoQ10) is intracellular antioxidant and mitochondrial membrane stabilizer.

show abstract

Section: Discussionsupporting

confidence: 91%

Comparative Study on the Influence of Epigallocatechin-3-gallat e and/ or Coenzyme Q10 against Alzheimer's disease Induced by Aluminium in Normally-Fed and Protein Malnourished Rats

Ali¹,

Ahmed²

2016

J Alzheimers Dis Parkinsonism

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“…26) Similarly, Kaizer et al investigated to determine whether long-term exposure to aluminum affects AchE activity in different mouse brain regions. 27) Long-term oral administration of aluminum (along with citrate supplementation for better absorption) increased AchE activity in all the investigated brain regions (the cortex, striatum, hippocampus, and hypothalamus), and the authors concluded that alteration of the lipid membrane might be a decisive factor in the modulation of AchE activity. As shown in the Fig.…”

Section: Discussionmentioning

confidence: 99%

Effects of Methoxsalen fromPoncirus trifoliataon Acetylcholinesterase and Trimethyltin-Induced Learning and Memory Impairment

Kim¹,

Choi²,

Bae³

et al. 2011

Bioscience, Biotechnology, and Biochemistry

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“…Moreover, the elevated level of MDA in the brain following a high paracetamol dose correlates with an increased rate of lipid peroxidation which is one of the main manifestations of oxidative damage (Sener et al, 2003). The elevated AChE activity could be attributed to neuronal membrane damage due to increased lipid peroxidation (Kaizer et al, 2005). Importantly, the increased AChE activity following administration of high doses of paracetamol will positively reduce the cholinergic neurotransmission efficiency by decreasing the level of acetylcholine in the synaptic cleft, but, on the other hand, may lead to an oxidative stress-mediated structural alteration in neurons.…”

Section: Discussionmentioning

confidence: 99%

Paracetamol Overdose Induces Physiological and Pathological Aberrations in Rat Brain

2017

J App Pharm Sci

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Paracetamol (Acetaminophen) is one of the most popular over the counter medications that is commonly used as an anti-inflammatory and pain killer, and to relieve fever and headaches. Despite its several therapeutic benefits, it is well known that an overdose of paracetamol can lead to hepatic and renal damage. Considering that brain cells is one of the main targets for paracetamol in the body, the effect of paracetamol on the physiology and histology of the brain is been poorly investigated. Hence, the present work investigates the possible adverse effects of paracetamol on the rat brain. Our results show that an overdose treatment of paracetamol caused significant elevation in the activity of AChE and a remarkable suppression in levels of dopamine and serotonin in treated rats. Also, applying rapid Golgi-cox staining showed that paracetamol induced morphological aberrations and a dramatic reduction in the density of dendritic spines in brain cells. Histological and ultrastructure alterations were also recorded in the neurons of paracetamol-treated rats. In conclusion, we found that an overdose of paracetamol is neurotoxic. The observed alterations point to the possibilities of higher brain impairments which is of strong public health concern.

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Acetylcholinesterase activation and enhanced lipid peroxidation after long-term exposure to low levels of aluminum on different mouse brain regions

Cited by 137 publications

References 35 publications

Comparative Study on the Influence of Epigallocatechin-3-gallat e and/ or Coenzyme Q10 against Alzheimer's disease Induced by Aluminium in Normally-Fed and Protein Malnourished Rats

Comparative Study on the Influence of Epigallocatechin-3-gallat e and/ or Coenzyme Q10 against Alzheimer's disease Induced by Aluminium in Normally-Fed and Protein Malnourished Rats

Effects of Methoxsalen fromPoncirus trifoliataon Acetylcholinesterase and Trimethyltin-Induced Learning and Memory Impairment

Paracetamol Overdose Induces Physiological and Pathological Aberrations in Rat Brain

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