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Anti-oxidant effect of ascorbic and dehydroascorbic acids in hippocampal slice culture
Eun Jin Kim1, Ran Won, Jin-Hun Sohn
1Department of Physiology, Brain Research Institute, Brain Korea 21 Project for Medical Science, Yonsei University College of Medicine, C.P.O. Box 8044, Seoul 120-752, Republic of Korea.
Biochemical and Biophysical Research Communications
|November 27, 2007
Summary
Ascorbic acid (AA) and dehydroascorbic acid (DHA) offer neuroprotection against kainic acid (KA) induced injury. Intermediate doses prevent neuronal death by inhibiting reactive oxygen species and mitochondrial dysfunction.
Area of Science:
- Neuroscience
- Biochemistry
- Cell Biology
Background:
- Ascorbic acid (AA) and dehydroascorbic acid (DHA) are known antioxidants with demonstrated protective effects in experimental models of neurological disorders like stroke and seizures.
- Kainic acid (KA) is a neurotoxin frequently used to induce excitotoxicity and neuronal damage, particularly in the hippocampus.
Purpose of the Study:
- To investigate the neuroprotective potential of ascorbic acid (AA) and dehydroascorbic acid (DHA) against kainic acid (KA)-induced neurotoxicity.
- To determine the dose-dependent effects of AA and DHA on neuronal survival and cellular dysfunction in an in vitro model.
Main Methods:
- Organotypic hippocampal slice cultures were utilized as an experimental model.
- Cultures were treated with kainic acid (KA) to induce neurotoxicity.
- Pretreatment with varying doses of ascorbic acid (AA) and dehydroascorbic acid (DHA) was administered prior to KA exposure.
- Neuronal death, reactive oxygen species (ROS) levels, and mitochondrial dysfunction were assessed.
Main Results:
- Kainic acid (KA) treatment led to significant delayed neuronal death in the CA3 region of hippocampal slices after 12 hours.
- Pretreatment with intermediate doses of both AA and DHA significantly reduced KA-induced neuronal death.
- Intermediate doses of AA and DHA also inhibited the generation of reactive oxygen species (ROS) and prevented mitochondrial dysfunction in the CA3 region.
- Low or high doses of AA and DHA did not show significant neuroprotective effects.
Conclusions:
- Ascorbic acid (AA) and dehydroascorbic acid (DHA) exhibit dose-dependent neuroprotective effects against kainic acid (KA)-induced neuronal injury.
- The neuroprotective mechanism involves the inhibition of reactive oxygen species (ROS) generation and the preservation of mitochondrial function.
- Intermediate concentrations of AA and DHA are crucial for achieving these beneficial effects in the context of KA neurotoxicity.
