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Interrelationships between astrocyte function, oxidative stress and antioxidant status within the central nervous
S Peuchen1, J P Bolaños, S J Heales
1Department of Neurochemistry, Institute of Neurology, London, U.K. s.peuchen@ion.ucl.ac.uk
Progress in Neurobiology
|July 1, 1997
Summary
Astrocytes are vital brain cells, not just support. They manage neuroactive compounds and combat oxidative stress using pathways like the glutathione system.
Area of Science:
- Neuroscience
- Cell Biology
- Neurophysiology
Background:
- Astrocytes were traditionally viewed as passive support cells in the central nervous system.
- Emerging evidence highlights their active and critical roles in brain physiology.
- Astrocytes possess receptors and transporters for neuroactive compounds, indicating complex signaling functions.
Purpose of the Study:
- To explore the multifaceted roles of astrocytes in central nervous system physiology.
- To investigate the impact of oxidative stress, particularly nitric oxide, on astrocytes and neurons.
- To examine the antioxidant defense mechanisms employed by astrocytes, focusing on the glutathione system.
Main Methods:
- Review of current literature on astrocyte function and neurobiology.
- Analysis of astrocyte receptor and transporter expression.
- Discussion of nitric oxide's dual role as a messenger and neurotoxin.
- Examination of astrocyte antioxidant pathways, emphasizing glutathione.
Main Results:
- Astrocytes actively participate in brain function through receptor and transporter interactions.
- Nitric oxide significantly impacts astrocyte and neuronal physiology, with potential for neurotoxicity.
- Astrocytes possess robust antioxidant capabilities, notably through the glutathione system, to mitigate oxidative stress.
Conclusions:
- Astrocytes are integral to brain function, involved in complex signaling and metabolic regulation.
- Understanding astrocyte responses to oxidative stress is crucial for neuroprotection.
- The glutathione system in astrocytes provides a powerful defense against free radical damage.