Synergistic effects of low level stressors in an oxidative damage model of spinal motor neuron degeneration

BACKGROUND : An increase in reactive oxygen species (ROS) burden and subsequent oxidative damage to nucleic acids, proteins, and lipids, occurs during the normal aging process of cells, including neurons. OBJECTIVE : With this in mind we hypothesize that an oxidative stress which leads to an increas...

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Bibliographic Details
Published in:Amyotrophic lateral sclerosis and other motor neuron disorders 2002-01, Vol.3 (3), p.151-157
Main Authors: Kriscenski-Perry, Elizabeth, Durham, Heather D, Sheu, Shey-Shing, Figlewicz, Denise A
Format: Article
Language:English
Subjects:
Amyotrophic Lateral Sclerosis
Animals
Cell Death
Cells, Cultured
Dose-Response Relationship, Drug
Drug Synergism
Embryo, Mammalian
Ganglia, Spinal - drug effects
Ganglia, Spinal - metabolism
Ganglia, Spinal - pathology
Glutamate Toxicity
Glutamic Acid - toxicity
Heat Shock
Heating
Mice
Motor Neurons
Motor Neurons - metabolism
Motor Neurons - pathology
Nerve Degeneration - metabolism
Nerve Degeneration - pathology
Oxidation-Reduction
Oxidative Stress
Paraquat - toxicity
Receptors, Kainic Acid - agonists
Spinal Cord - drug effects
Spinal Cord - metabolism
Spinal Cord - pathology
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Summary:BACKGROUND : An increase in reactive oxygen species (ROS) burden and subsequent oxidative damage to nucleic acids, proteins, and lipids, occurs during the normal aging process of cells, including neurons. OBJECTIVE : With this in mind we hypothesize that an oxidative stress which leads to an increased state of oxidation, but is not itself lethal, nonetheless renders the motor neuron more vulnerable to other sublethal stressors. METHOD AND RESULTS : We have combined paraquat-induced oxidative stress with sublethal increased exogenous glutamate, or thermal stress, or a combination of both, and demonstrate a synergistic effect of low-level stressors on the viability of motor neurons. CONCLUSION : This model of low-level oxidative stress reveals the subsequent vulnerability of motor neurons to genetic or environmental stressors and may in part explain the mid-life/late-life symptom onset in both familial and sporadic ALS patients.
ISSN:1466-0822
DOI:10.1080/146608202760834166