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Decreased membrane fluidity and hyperpolarization in aluminum-treated PC-12 cells correlates with increased production of cellular oxidants.

Authors
Johnson-VJ; Tsunoda-M; Murray-TF; Sharma-RP
Source
Environ Toxicol Pharmacol 2005 Feb; 19(2):221-230
NIOSHTIC No.
20026185
Abstract
Effects of aluminum (Al) on membrane properties of excitable cells are not fully understood. Several reports have identified cellular membranes as sensitive targets for Al intoxication. In the present study, we tested the hypothesis that treatment with Al would alter membrane fluidity and potential and these changes would correlate with aberrant generation of cellular oxidants. The effects of in vitro Al exposure in resting rat pheochromocytoma (PC-12) cells, a model that exhibits neuron-like properties, were investigated. Treatment of PC-12 cells with Al (>0.01 mM) resulted in a concentration-dependent decrease in membrane fluidity. Similar concentrations of Al increased the rate of extracellular acidification, measured by a cytosensor microphysiometer, indicating stimulation of proton extrusion from cells. This change in proton extrusion was accompanied by a rapid and concentration-dependent hyperpolarizion of the cell membrane as determined by decreased fluorescence of a potential-sensitive dye, bis-[1,3-dibutylbarbituric acid]trimethine oxonol [Dibac4(3)]. Al-induced perturbations of membrane properties correlated with an increased level of cellular oxidants, indicated by increasing dihydrorhodamine 123 oxidation. Results suggest that acute exposure to Al modifies membrane properties of neuron-like cells and therefore cellular membranes represent a plausible target for Al neurotoxicity. Alterations in membrane potential can have a dramatic impact on cellular communication especially in neurons and may be an important mechanism in Al neurotoxicity.
Keywords
Aluminum-compounds; Oxidation; In-vitro-studies; Exposure-levels; Laboratory-animals; Animals; Animal-studies; Models; Cell-cultures; Acute-exposure; Acute-toxicity; Neurotoxicity
CODEN
ETOPFR
CAS No.
7429-90-5
Publication Date
20050201
Document Type
Journal Article
Email Address
rpsharma@vet.uga.edu
Fiscal Year
2005
NTIS Accession No.
NTIS Price
Issue of Publication
2
ISSN
1382-6689
NIOSH Division
HELD
Priority Area
Disease and Injury: Asthma and Chronic Obstructive Pulmonary Disease
Source Name
Environmental Toxicology and Pharmacology
State
WV; GA
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