Effect of Long-Term Exposure to Aluminum on the Acetylcholinesterase Activity in the Central Nervous System and Erythrocytes

Kaizer, Rosilene Rodrigues; Junior, Marcos Corrêa; Gris, Lara Regina Soccol; Rosa, Cláudia Severo da; Bohrer, Denise; Morsch, Vera Maria; Schetinger, Maria Rosa Chitolina

doi:10.1007/s11064-008-9725-6

Cited by 78 publications

(52 citation statements)

References 46 publications

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“…Zhang et al [48] reported increased AchE activity in Al overloaded rats. Kaizer et al [49] suggested that Al exposure increased AchE activity via allosteric interaction between Al and the peripheral anionic site of the enzyme molecule, leading to the etiology of AD pathological deterioration.…”

Section: Discussionmentioning

confidence: 99%

Does Melatonin Ameliorate Neurological Changes Associated With Alzheimer’s Disease in Ovariectomized Rat Model?

et al. 2012

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This study aimed to elucidate the mechanisms of melatonin to manage neurological damage in Alzheimer's disease (AD) induced in ovariectomized rats. Forty adult female rats were enrolled in our study and were classified as; gonad intact control, ovariectomized control group, ovariectomized rats received melatonin, ovariectomized rats injected with AlCl 3 to induce AD and ADinduced rats treated with melatonin. Hydrogen peroxide (H 2 O 2 ), malondialdehyde (MDA), total antioxidant capacity (TAC), superoxide dismutase (SOD), catalase (CAT), B cell lymphoma 2 (Bcl-2), brain derived neurotrophic factor (BDNF), acetylcholinesterase (AchE) and acetylcholine (Ach) were estimated in the brain tissues of the different groups. Treatment of AD-induced rats with melatonin produced marked improvement in the most studied biomarkers which was confirmed by histological investigation of the brain. In Conclusion, melatonin significantly ameliorates the neurodegeneration characteristic of AD in experimental animal model due to its antioxidant, antiapoptotic, neurotrophic and anti-amyloidogenic activities.

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Section: Discussionmentioning

confidence: 99%

Does Melatonin Ameliorate Neurological Changes Associated With Alzheimer’s Disease in Ovariectomized Rat Model?

et al. 2012

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“…Also, Al can interact with plasma membrane lipids and affect the activity of membrane associated enzymes, including AChE. The increase in the brain AChE activity following aluminium exposure of rats was attributed to an allosteric interaction between Al with the peripheral anionic site of the enzyme molecule (50). The ability of eugenol to directly suppress the enhanced AChE activity following Al intoxication in the current study could be explained with the finding of an in vitro study that demonstrated a potential anti-cholinesterase property of eugenol (51).…”

Section: Figure 3 Effect Of Eugenol And/or Aluminium On Brain Acetylcmentioning

confidence: 99%

Neuroprotective effects of eugenol against aluminiuminduced toxicity in the rat brain

Said

Rabo

2017

Archives of Industrial Hygiene and Toxicology

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Aluminium (Al) is a neurotoxic metal that contributes to the progression of several neurodegenerative diseases. The aim of the present study was to evaluate the protective effect of dietary eugenol supplementation against aluminium (Al)- induced cerebral damage in rats. Male Wistar rats were divided into four groups: normal controls, rats fed a diet containing 6,000 μg g-1 eugenol, rats intoxicated daily with aluminium chloride (84 mg kg-1 body weight) p. o. and fed either a basal diet or a eugenol-containing diet. Daily oral administration of Al for four consecutive weeks to rats significantly reduced brain total antioxidant status (TAS) (11.42±0.31 μmol g-1 tissue, p<0.001) with a subsequent significant enhancement of lipid peroxidation (MDA) (32.55±1.68 nmol g-1 tissue, p<0.002). In addition, Al enhanced brain acetylcholinesterase activity (AChE) (46.22±4.90 U mg-1 protein, p<0.001), tumour necrosis factor alpha (TNF-α) (118.72±11.32 pg mg-1 protein, p<0.001), and caspase 3 (Casp-3) (8.77±1.26 ng mg-1 protein, p<0.001) levels, and in contrast significantly suppressed brain-derived neurotrophic factor (BDNF) (82.74±14.53 pg mg-1 protein, p<0.002) and serotonin (5-HT) (1.54±0.12 ng mg-1 tissue, p<0.01) levels. Furthermore, decreased glial fibrillary acidic protein (GFAP) immunostaining was noticed in the striatum of Al-intoxicated rats, compared with untreated controls. On the other hand, co-administration of dietary eugenol with Al intoxication restored brain BDNF (108.76±2.64 pg mg-1 protein) and 5-HT (2.13±0.27 ng mg-1 tissue) to normal levels, enhanced brain TAS (13.43±0.24 μmol g-1 tissue, p<0.05), with a concomitant significant reduction in TNF-α (69.98±4.74 pg mg-1 protein) and Casp-3 (3.80±0.37 ng mg-1 protein) levels (p<0.001), as well as AChE activity (24.50±3.25 U mg-1 protein, p<0.001), and increased striatal GFAP immunoreactivity, compared with Al-treated rats. Histological findings of brain tissues verified biochemical data. In conclusion, eugenol holds potential as a neuroprotective agent through its hydrophobic, antioxidant, and anti-apoptotic properties, as well as its neurotrophic ability against Al-induced brain toxicity in rats.

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“…Aluminum can act as a neurotoxin and it has been investigated as the causative agent of Alzheimer's disease for many years; however, no decisive connection has been found 115,116 . Contradictory changes in brain AChE activity after aluminum exposure have been found in different brain regionss 117,118 . On the other hand, AChE is not only affected by aluminum.…”

Section: Inhibitors Of Peripheral (β) Anionic Sitementioning

confidence: 99%

Cholinesterases, a Target of Pharmacology and Toxicology

Pohanka¹

2011

Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub

319

219

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Background. Cholinesterases are a group of serine hydrolases that split the neurotransmitter acetylcholine (ACh) and terminate its action. Of the two types, butyrylcholinesterase and acetylcholinesterase (AChE), AChE plays the key role in ending cholinergic neurotransmission. Cholinesterase inhibitors are substances, either natural or man-made that interfere with the break-down of ACh and prolong its action. Hence their relevance to toxicology and pharmacology.Methods and Results. The present review summarizes current knowledge of the cholinesterases and their inhibition. Particular attention is paid to the toxicology and pharmacology of cholinesterase-related inhibitors such as nerve agents (e.g. sarin, soman, tabun, VX), pesticides (e.g. paraoxon, parathion, malathion, malaoxon, carbofuran), selected plants and fungal secondary metabolites (e.g. aflatoxins), drugs for Alzheimer's disease (e.g. huperzine, metrifonate, tacrine, donepezil) and Myasthenia gravis (e.g. pyridostigmine) treatment and other compounds (propidium, ethidium, decamethonium).Conclusions. The crucial role of the cholinesterases in neural transmission makes them a primary target of a large number of cholinesterase-inhibiting drugs and toxins. In pharmacology, this has relevance to the treatment of neurodegenerative disorders.

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Effect of Long-Term Exposure to Aluminum on the Acetylcholinesterase Activity in the Central Nervous System and Erythrocytes

Cited by 78 publications

References 46 publications

Does Melatonin Ameliorate Neurological Changes Associated With Alzheimer’s Disease in Ovariectomized Rat Model?

Does Melatonin Ameliorate Neurological Changes Associated With Alzheimer’s Disease in Ovariectomized Rat Model?

Neuroprotective effects of eugenol against aluminiuminduced toxicity in the rat brain

Cholinesterases, a Target of Pharmacology and Toxicology

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