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Updated: May 12, 2026
09:53
Screening Assay for Oxidative Stress in a Feline Astrocyte Cell Line, G355-5
Published on: July 13, 2011
Hemoglobin-mediated oxidant damage to the central nervous system requires endogenous ascorbate
1Department of Laboratory Medicine/Pathology, University of Minnesota, Minneapolis 55455.
The Journal of Clinical Investigation
|November 1, 1988
Summary
Central nervous system (CNS) hemorrhage can cause seizures and paralysis. Hemoglobin
Area of Science:
- Neuroscience
- Biochemistry
- Pathology
Background:
- Hemorrhage in the central nervous system (CNS) is linked to seizures and paralysis.
- Hemoglobin released from red blood cells may be toxic to the CNS via lipid peroxidation and Na,K-ATPase inhibition.
- Previous studies suggest free iron from hemoglobin contributes to these toxic effects.
Purpose of the Study:
- To investigate the role of CNS components in mediating hemoglobin-induced neurotoxicity.
- To identify the reducing substance responsible for blocking iron-mediated CNS lipid oxidation.
Main Methods:
- Utilized Fe2+ and Fe3+ chelators (ferene, desferrioxamine) to assess iron's role.
- Measured CNS lipid oxidation in murine brain homogenates.
- Employed ascorbate oxidase to test the involvement of ascorbic acid.
- Washed CNS membranes and added ascorbate to evaluate its effect on peroxidation.
Main Results:
- Ferene inhibited ferric iron-mediated CNS lipid oxidation, indicating Fe3+ reduction within the CNS.
- Ascorbic acid was identified as the reducing substance responsible for blocking hemoglobin/iron-driven peroxidation.
- Washing CNS membranes or using ascorbate oxidase prevented peroxidation, while adding ascorbate restored it.
Conclusions:
- Posthemorrhagic CNS dysfunction may result from redox reactions involving hemoglobin iron, ascorbic acid, and CNS lipids.
- Ascorbic acid plays a critical role in the neurotoxic effects of hemoglobin following CNS hemorrhage.
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