Aluminium in rat cerebellar primary cultures

G, De Stasio; Mercanti, Delio; Mt, Ciotti; Dunham, D G; Droubay, Timothy C.; Bp, Tonner; Perfetti, P.; Margaritondo, G.

doi:10.1097/00001756-199410000-00034

Cited by 21 publications

(19 citation statements)

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“…However, the target of aluminum toxicity is not known exactly; in neurons bundling of neurofilaments was described in the somata and the neurites (Katsetos et al 1990;Gilbert et al 1992;Theiss and Meller 2001). In addition, several investigations indicate that aluminum is preferentially taken up by glial cells of the CNS (Albrecht et al 1991;Rao 1992;Campbell et al 1999), where it is found in the outermost flat portions of the cell bodies, rather than in their central, thicker parts (De Stasio et al 1994). Our fluorescence-microscopic investigations as well as the ultrastructural data of an abnormal distribution and structure of the cytoskeleton in astrocytes exposed to aluminum are in line with these findings.…”

Section: Effects Of Aluminum Exposure On Cultured Astrocytessupporting

confidence: 89%

Aluminum impairs gap junctional intercellular communication between astroglial cells in vitro

Theiß

Meller

2002

Cell and Tissue Research

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The purpose of the present study was to investigate the effect of aluminum on gap junctional intercellular communication (GJIC) in cultured astrocytes. In the CNS the extracellular environment and metabolic status of neurons is dependent upon astrocytes, which are known to exhibit GJIC. This cell-to-cell communication provides a cytoplasmic continuity between adjacent cells, allowing exchange of diverse ions, second messengers, and metabolites. To study the effects of aluminum intoxication on GJIC in cultured glial cells, astroglial cell cultures obtained from fetal rat brains were exposed to aluminum lactate for 2-6 weeks. To demonstrate the metabolic coupling of neighboring cells, the technique of microinjection of the gap junction permeable substance neurobiotin was performed. Whereas in controls intensive GJIC was observed by dye transfer of neurobiotin from the microinjected cell into the adjacent astrocytes, aluminum treatment significantly impaired this cellular communication. As aluminum is known to affect cytoskeletal elements, additional investigations into the organization of intermediate filaments (glial fibrillary acid protein, GFAP) and microfilaments in control astrocytes and subsequent aluminum exposure were performed with the aid of fluorescence microscopy and rapid-freeze, deep-etch electron microscopy. Aluminum exposure led to an aggregation of GFAP-positive filaments near to the cell nucleus, accompanied by a destruction of the actin cytoskeleton, especially close to the cell membrane. Ultrastructurally these data could be verified as prominent areas without actin filaments contacting the cell membrane detectable in aluminum-treated astrocytes. Immunohistochemical staining of Cx43 revealed an impaired trafficking of this connexin into the cell prolongations following aluminum treatment, although electron-microscopic data revealed that gap junctions between adjacent astrocytes were still present after aluminum incubation for 24 days. In conclusion, in cultured astrocytes the morphological integrity of microfilaments and the intermediate filament network seem to be fundamental for the translocation of connexins from Golgi complex into the cellular prolongation to exhibit proper and extensive cellular communication through gap junctions.

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Section: Effects Of Aluminum Exposure On Cultured Astrocytessupporting

confidence: 89%

Aluminum impairs gap junctional intercellular communication between astroglial cells in vitro

Theiß

Meller

2002

Cell and Tissue Research

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“…In both cases, post-mortem determinations of aluminium content in brain samples showed aluminium concentration ranging from 0.75 lg g À1 (frontal white matter) to 49 lg g À1 (choroid plexus). It is known that aluminium can cross the blood-brain barrier [35,36] and accumulates in nerve [37][38][39][40][41][42][43][44] and glial cells [39][40][41][42][43]45], reaching up to micromolar concentrations within the cells.…”

Section: Backward-looking To Neurotoxicitymentioning

confidence: 99%

Does neurotransmission impairment accompany aluminium neurotoxicity?

Gonçalves

Silva

2007

Journal of Inorganic Biochemistry

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“…Once within the brain, aluminium is distributed within the neurons and glial cells (DeStasio et al 1994;Campbell et al 1999), thus causing various alterations. Its close association to Alzheimer's disease (AD) (Flaten 2001) has renewed the interest in aluminium-induced neurotoxicity.…”

Section: Introductionmentioning

confidence: 99%

Aluminium-Induced Imbalance in Oxidant and Antioxidant Determinants in Brain Regions of Female Rats: Protection by Centrophenoxine

Nehru¹,

Bhalla²

2006

Toxicology Mechanisms and Methods

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The present study was carried out to investigate the potential of centrophenoxine in modulating aluminium-induced neurotoxicity. Female Sprague Dawley rats were administered aluminium chloride orally (40 mg/kg b.w./day) for a period of 8 weeks. At the end of respective treatment, various markers of oxidative stress were determined in four different regions of brain: cerebrum cerebellum, medulla oblongata, and hypothalamus. Lipid peroxidation assay was also carried out using standard techniques. Simultaneously, the centrophenoxine group (100 mg/kg b.w./day) for 6 weeks was also run long to understand the role in ameliorating oxidative damage. A significant decrease in the activities of superoxide dismutase and catalase was noticed in all the four regions, the most significant being in the hypothalamus (0.603 +/- .06) and cerebrum (0.038 +/- .01). Due to aluminium toxicity, peroxidation of lipids was also found to be elevated in cerebrum (0.424 +/- .03), cerebellum (0.341 +/- .03), hypothalamus (1.018 +/- .007), and medulla oblongata (0.304 +/- .05). However, posttreatment with centrophenoxine significantly elevated the superoxide and catalase activities in different regions. In addition, lipid peroxidation status of membranes was significantly reduced after centrophenoxine posttreatment to aluminium-exposed animals. Centrophenoxine has proved to be beneficial in combating the damage caused by aluminium toxicity. However, further research is needed to have a better understanding of the molecular basis of aluminium-induced oxidative damage. In addition, the different aspects of centrophenoxine need to be unmasked.

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Aluminium in rat cerebellar primary cultures

Cited by 21 publications

References 0 publications

Aluminum impairs gap junctional intercellular communication between astroglial cells in vitro

Aluminum impairs gap junctional intercellular communication between astroglial cells in vitro

Does neurotransmission impairment accompany aluminium neurotoxicity?

Aluminium-Induced Imbalance in Oxidant and Antioxidant Determinants in Brain Regions of Female Rats: Protection by Centrophenoxine

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