Brain Oxidative Stress and Selective Behaviour of Aluminium In Specific Areas of Rat Brain: Potential Effects In a 6-OHDA-Induced Model of Parkinson's Disease (original) (raw)
Related papers
Neurotoxicity of Aluminium: A Comprehensive Review
International Journal of Biology, Pharmacy and Allied Sciences, 2020
Aluminium is one of the major environmental neurotoxin, whose exposure produces several adverse effects. The severity of damage depends on the time and levels of exposure, the rate of absorption, individual susceptibility and the route by which the metal is absorbed. Aluminium has been reported that it can lead to Alzheimer's disease despite the controversy around the issue. When aluminum is absorbed into your brain, it lasts over a very long period and the half-life is reported to be 20% of lifetime. Although the precise cause of aluminium toxicity is unclear, the studies indicate that aluminium can enhance the inflammatory and oxidative events resulting in the synthesis of reactive oxygen-species and the degradation of antioxidant defense enzymes, which contribute to increased mitochondrial oxidative stress. This review attempts to describe the causes of exposure, symptoms of toxicity and molecular mechanisms by which neurotoxins can cause neurotoxicity, prevention and treatment for the aluminium induced neurotoxicity.
Multifaceted effects of aluminium in neurodegenerative diseases: A review
Biomedicine & Pharmacotherapy, 2016
Aluminium (Al) is the most common metal and widely distributed in our environment. Al was first isolated as an element in 1827, and its use began only after 1886. Al is widely used for industrial applications and consumer products. Apart from these it is also used in cooking utensils and in pharmacological agents, including antacids and antiperspirants from which the element usually enters into the human body. Evidence for the neurotoxicity of Al is described in various studies, but still the exact mechanism of Al toxicity is not known. However, the evidence suggests that the Al can potentiate oxidative stress and inflammatory events and finally leads to cell death. Al is considered as a well-established neurotoxin and have a link between the exposure and development of neurodegenerative diseases, including Amyotrophic Lateral Sclerosis (ALS), Alzheimer's disease (AD), dementia, Gulf war syndrome and Parkinsonism. Here, we review the detailed possible pathogenesis of Al neurotoxicity. This review summarizes Al induced events likewise oxidative stress, cell mediated toxicity, apoptosis, inflammatory events in the brain, glutamate toxicity, effects on calcium homeostasis, gene expression and Al induced Neurofibrillary tangle (NFT) formation. Apart from these we also discussed animal models that are commonly used for Al induced neurotoxicity and neurodegeneration studies. These models help to find out a better way to treat and prevent the progression in Al induced neurodegenerative diseases.
Does neurotransmission impairment accompany aluminium neurotoxicity?
Journal of inorganic biochemistry, 2007
Neurobehavioral disorders, except their most overt form, tend to lie beyond the reach of clinicians. Presently, the use of molecular data in the decision-making processes is limited. However, as details of the mechanisms of neurotoxic action of aluminium become clearer, a more complete picture of possible molecular targets of aluminium can be anticipated, which promises better prediction of the neurotoxicological potential of aluminium exposure. In practical terms, a critical analysis of current data on the effects of aluminium on neurotransmission can be of great benefit due to the rapidly expanding knowledge of the neurotoxicological potential of aluminium. This review concludes that impairment of neurotransmission is a strong predictor of outcome in neurobehavioral disorders. Key questions and challenges for future research into aluminium neurotoxicity are also identified.
Molecular mechanisms of aluminum neurotoxicity: Update on adverse effects and therapeutic strategies
Neurotoxicity of Metals: Old Issues and New Developments, 2021
HAL is a multidisciplinary open access archive for the deposit and dissemination of scientific research documents, whether they are published or not. The documents may come from teaching and research institutions in France or abroad, or from public or private research centers. L'archive ouverte pluridisciplinaire HAL, est destinée au dépôt et à la diffusion de documents scientifiques de niveau recherche, publiés ou non, émanant des établissements d'enseignement et de recherche français ou étrangers, des laboratoires publics ou privés.
Aluminium Induces Iron-Mediated Oxidative Stress in Brain Tissue
BJSTR, 2022
Numerous studies have confirmed a link between aluminium (Al) and neurodegenerative disorders. In this study, the toxic effects of aluminium ions on the brain were investigated after a 14-day sub-acute exposure of Balb/c mice to 0.1 LD50 Al3+. The exposure to Al3+ caused an increase in malondialdehyde, a marker of lipid peroxidation, and a decrease in total glutathione, a marker of intracellular redox status, concentrations in the brain. To elucidate the reason of oxidative stress in the brain, concentrations of Al ions and biomarkers of redox status and iron homeostasis were measured in the blood serum of mice.
Aluminium and Neuro-degeneration: Mechanism of Pathogenesis and Possible Strategies for Mitigation
One of the most abundant metal in our environment is aluminium (Al). Occupational exposure of humans to Al takes place during its extractions, processing and fabrications of articles of daily use. Al in drinking water and as well as its use in packaging & storage of food is also a potential source of exposure. Acute exposure of higher concentration or chronic exposure of low concentration of Al leads to its aggregation in various parts of the body, resulting in system toxicity. Brain is highly susceptible to Al accumulation toxicity. In humans, exposure of Al is a risk factor for the starting of Alzheimer Disease. The adverse effect of Al exposure on nervous system results in memory loss, balance problems and impairment of coordination. High level of Al in brain increases lipid peroxidation and oxidative stress and reduces antioxidant enzymes level. It also causes aggregation of amyloid beta proteins and formation of Neurofibrillary Tangles (NFTs) of tau proteins which finally leads to death of neuronal cell and neurotoxicity. Metabolism and excretion of heavy metals including Al is very difficult and its leads to accumulation. The chelation therapy has been proposed where the organic molecules like EDTA, Chlorogenic acid and GSH binds with the heavy metals and facilitates for their excretion from body. However, non-specific binding of these chelators is another major safety concern. Medicinal plants and their phytochemicals with multiple mechanism of action have been proposed as a very good alternative for ameliorating heavy metal induced toxicity. In addition to mild chelating activities, the phytochemicals have antioxidant, anti-inflammatory, cytokine modulatory and other specific actions for proving holistic neuro-protection on heavy metal exposure.
Metabolic Brain Disease
The conceptualisation of autistic spectrum disorder and Alzheimer's disease has undergone something of a paradigm shift in recent years and rather than being viewed as single illnesses with a unitary pathogenesis and pathophysiology they are increasingly considered to be heterogeneous syndromes with a complex multifactorial aetiopathogenesis, involving a highly complex and diverse combination of genetic, epigenetic and environmental factors. One such environmental factor implicated as a potential cause in both syndromes is aluminium, as an element or as part of a salt, received, for example, in oral form or as an adjuvant. Such administration has the potential to induce pathology via several routes such as provoking dysfunction and/or activation of glial cells which play an indispensable role in the regulation of central nervous system homeostasis and neurodevelopment. Other routes include the generation of oxidative stress, depletion of reduced glutathione, direct and indirect reductions in mitochondrial performance and integrity, and increasing the production of proinflammatory cytokines in both the brain and peripherally. The mechanisms whereby environmental aluminium could contribute to the development of the highly specific pattern of neuropathology seen in Alzheimer's disease are described. Also detailed are several mechanisms whereby significant quantities of aluminium introduced via immunisation could produce chronic neuropathology in genetically susceptible children. Accordingly, it is recommended that the use of aluminium salts in immunisations should be discontinued and that adults should take steps to minimise their exposure to environmental aluminium.
Molecular toxicity of aluminium in relation to neurodegeneration
The Indian journal of medical research, 2008
Exposure to high levels of aluminium (Al) leads to neurofibrillary degeneration and that Al concentration is increased in degenerating neurons in Alzheimer's disease (AD). Nevertheless, the role of Al in AD remains controversial and there is little proof directly interlinking Al to AD. The major problem in understanding Al toxicity is the complex Al speciation chemistry in biological systems. A new dimension is provided to show that Al-maltolate treated aged rabbits can be used as a suitable animal model for understanding the pathology in AD. The intracisternal injection of Al-maltolate into aged New Zealand white rabbits results in pathology that mimics several of the neuropathological, biochemical and behavioural changes as observed in AD. The neurodegenerative effects include the formation of intraneuronal neurofilamentous aggregates that are tau positive, oxidative stress and apoptosis. The present review discusses the role of Al and use of Al-treated aged rabbit as a suitab...