Iron Dyshomeostasis Participated in Rat Hippocampus Toxicity Caused by Aluminum Chloride

Zhang, Jian; Huang, Wanyue; Xu, Feibo; Cao, Zheng; Jia, Fubo; Li, Yanfei

doi:10.1007/s12011-019-02008-7

Cited by 19 publications

(10 citation statements)

References 52 publications

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“…[39][40][41] Al may bind with superoxide anions and form Al-superoxide anions and these oxidants can lead to reduced activity of mitochondrial superoxide dismutase. 4,6 In the Al treated rats, significantly increased MDA level and decreased CAT, SOD activities were noticed. Further, chronic supplementation of naringin significantly enhanced the antioxidant enzyme activity (SOD, CAT) and reduced the level of MDA.…”

Section: Discussionmentioning

confidence: 93%

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Naringin Attenuates Aluminum Induced Cognitive Deficits in Rats

Orsu¹

2020

IJPER

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Aim: The exposure of aluminum for longer period in brain can lead to impaired cognition and behavioral changes. The present study was aimed to investigate the aluminum induced cognitive deficits and possible protective outcomes of naringin. Materials and Methods: Aluminum chloride in a dose of 100 mg/kg i.p was employed for 60 days to induce cognitive deficits in Westar rats. The animals were divided into groups each group contain six animals, as normal, aluminum treated, naringin treated (25, 50, 100 mg/kg). These animals were used to estimate behavioral characters such as Open field, eight arm radial maze, Morris water maze and Rota-rod tests and also used to assess the biochemical parameters such as acetylcholine esterase activity, malondialdehyde, superoxide dismutase and catalase. Results: Aluminum intoxicated rats showed significantly reduced exploratory and spontaneous locomotors activities in open field test and significant impairment in working and learning memory assessed by Morris water maze and radial arm maze tests. It also significantly increased acetylcholine esterase activity and malondialdehyde. The superoxide dismutase and catalase were also decreased significantly. Naringin was given (25, 50 and 100 mg/kg PO) to the aluminum intoxicated rats for a period of 30 days. The naringin treatment has shown significant improvements in spontaneous locomotors and exploratory activities and memory performance tasks of rats. Conclusion: The oxidative stress (reduced lipid peroxidation, restored reduced superoxide dismutase and catalase) and acetylcholine esterase activity were significantly decreased in the naringin group. Thus, these findings supported that naringin has showed potential neuroprotection against aluminum induced oxidative stress and cognitive deficit.

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Section: Discussionmentioning

confidence: 93%

“…Several researchers also demonstrated the Al intoxication in experimental animals and humans cause neurotoxicity and cognitive deficits. [1][2][3][4] Therefore, in this study Al intoxication in animals was considered as experimental model. Generally, memory process and learning process in the brain are maintained by the cholinergic system.…”

Section: Introductionmentioning

confidence: 99%

Naringin Attenuates Aluminum Induced Cognitive Deficits in Rats

Orsu¹

2020

IJPER

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“…The necrosis rates of the necrotic neurons out of the total neurons were manually counted along the ipsilateral of the hippocampal CA1 region [ 30 ].…”

Section: Methodsmentioning

confidence: 99%

Key Mechanisms and Potential Implications of Hericium erinaceus in NLRP3 Inflammasome Activation by Reactive Oxygen Species during Alzheimer’s Disease

et al. 2021

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Alzheimer’s disease (AD) is the principal cause of dementia, and its incidence increases with age. Altered antioxidant systems and inflammation have an important role in the etiology of neurodegenerative disorders. In this study, we evaluated the effects of Hericium erinaceus, a nutritional mushroom with important antioxidant effects, in a rat model of AD. Animals were injected with 70 mg/Kg of AlCl3 daily for 6 weeks, and Hericium erinaceus was administered daily by gavage. Before the experiment’s end date, behavioral test training was performed. At the end of the study, behavioral changes were assessed, and the animals were euthanized. Brain tissues were harvested for further analysis. AlCl3 mainly accumulates in the hippocampus, the principal region of the brain involved in memory functions and learning. Hericium erinaceus administration reduced behavioral changes and hippocampal neuronal degeneration. Additionally, it reduced phosphorylated Tau levels, aberrant APP overexpression, and β-amyloid accumulation. Moreover, Hericium erinaceus decreased the pro-oxidative and pro-inflammatory hippocampal alterations induced by AD. In particular, it reduced the activation of the NLRP3 inflammasome components, usually activated by increased oxidative stress during AD. Collectively, our results showed that Hericium erinaceus has protective effects on behavioral alteration and histological modification associated with AD due to the modulation of the oxidative and inflammatory pathways, as well as regulating cellular brain stress.

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“…In fact, Al is responsible for oxidative stress, cytotoxicity, genotoxicity, pro-inflammatory effects, immunological alterations, peptide denaturation or transformation, enzymatic dysfunctions, metabolic derangements, membrane disruption, microtubule perturbation, iron dyshomeostasis, amyloidogenesis, apoptosis, necrosis, and dysplasia [ 20 ]. Studies on animals have also shown that Al is neurotoxic and targets the central nervous system [ 11 , 19 , 21 , 22 , 23 , 24 ] by crossing the blood–brain barrier or by being transported through olfactory nerves [ 25 ]. In a rodent model, Al causes neurodegeneration, nerve cell death, changes in acetylcholinesterase (AChE) and neurotransmitter levels, histopathological changes (such as neuronal vacuolisation), and impaired cognitive and locomotor performances [ 12 , 24 , 25 , 26 , 27 , 28 ].…”

Section: Introductionmentioning

confidence: 99%

“…Studies on animals have also shown that Al is neurotoxic and targets the central nervous system [ 11 , 19 , 21 , 22 , 23 , 24 ] by crossing the blood–brain barrier or by being transported through olfactory nerves [ 25 ]. In a rodent model, Al causes neurodegeneration, nerve cell death, changes in acetylcholinesterase (AChE) and neurotransmitter levels, histopathological changes (such as neuronal vacuolisation), and impaired cognitive and locomotor performances [ 12 , 24 , 25 , 26 , 27 , 28 ]. In humans, it is known to be associated with many pathologies of the nervous system, such as Alzheimer’s and Parkinson’s diseases, dementia, and autism [ 20 ].…”

Section: Introductionmentioning

confidence: 99%

Effects of Aluminium Contamination on the Nervous System of Freshwater Aquatic Vertebrates: A Review

Closset

Cailliau

Slaby

et al. 2021

IJMS

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Aluminium (Al) is the most common natural metallic element in the Earth’s crust. It is released into the environment through natural processes and human activities and accumulates in aquatic environments. This review compiles scientific data on the neurotoxicity of aluminium contamination on the nervous system of aquatic organisms. More precisely, it helps identify biomarkers of aluminium exposure for aquatic environment biomonitoring in freshwater aquatic vertebrates. Al is neurotoxic and accumulates in the nervous system of aquatic vertebrates, which is why it could be responsible for oxidative stress. In addition, it activates and inhibits antioxidant enzymes and leads to changes in acetylcholinesterase activity, neurotransmitter levels, and in the expression of several neural genes and nerve cell components. It also causes histological changes in nerve tissue, modifications of organism behaviour, and cognitive deficit. However, impacts of aluminium exposure on the early stages of aquatic vertebrate development are poorly described. Lastly, this review also poses the question of how accurate aquatic vertebrates (fishes and amphibians) could be used as model organisms to complement biological data relating to the developmental aspect. This “challenge” is very relevant since freshwater pollution with heavy metals has increased in the last few decades.

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Iron Dyshomeostasis Participated in Rat Hippocampus Toxicity Caused by Aluminum Chloride

Cited by 19 publications

References 52 publications

Naringin Attenuates Aluminum Induced Cognitive Deficits in Rats

Naringin Attenuates Aluminum Induced Cognitive Deficits in Rats

Key Mechanisms and Potential Implications of Hericium erinaceus in NLRP3 Inflammasome Activation by Reactive Oxygen Species during Alzheimer’s Disease

Effects of Aluminium Contamination on the Nervous System of Freshwater Aquatic Vertebrates: A Review

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