Antioxidant Therapeutics in Neurotoxicity and Epilepsy

Oxidative stress is increasingly recognised as a key driver of neuronal injury in both acute neurotoxic insults and chronic epileptic conditions. Excessive generation of reactive oxygen species (ROS) during seizures or exposure to neurotoxic agents disrupts mitochondrial function, triggers lipid peroxidation and provokes neuroinflammation. Antioxidant therapeutics aim to restore redox balance, preserve neuronal integrity and modulate inflammatory cascades. Preclinical models demonstrate that small molecules, phytochemicals and repurposed drugs can bolster endogenous defence systems—upregulating enzymes such as superoxide dismutase and glutathione peroxidase, reducing lipid peroxidation by-products and stabilising mitochondrial membrane potential. In epilepsy, oxidative damage contributes to seizure propagation, gliosis and progressive cognitive decline; targeted antioxidants have shown promise in attenuating seizure frequency, dampening excitotoxicity and improving behavioural outcomes. Emerging strategies include direct free‐radical scavengers, modulators of redox‐sensitive transcription factors and agents that enhance mitochondrial biogenesis. These approaches hold potential for adjunctive therapy in drug-resistant epilepsy and for protection against environmental or pharmacological neurotoxins.

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Antioxidant Therapeutics in Neurotoxicity and Epilepsy publication trend

The graph below shows the total number of articles in antioxidant therapeutics in neurotoxicity and epilepsy across all publications each year (not limited to Nature Index journals).

Technical terms

Oxidative stress: imbalance between reactive oxygen species production and antioxidant defences leading to cellular damage.

Reactive oxygen species (ROS): chemically reactive oxygen-derived molecules that can oxidise lipids, proteins and nucleic acids.

Lipid peroxidation: oxidative degradation of lipids resulting in membrane dysfunction and toxic aldehyde formation.

Antioxidant enzyme: protein catalysts, such as superoxide dismutase and catalase, that neutralise ROS and limit oxidative injury.

Radical scavenging: chemical neutralisation of free radicals by antioxidant molecules to prevent chain reactions of oxidation.

References

1. Extraction, Phytochemical profile, and neuroprotective activity of Phyllanthus emblica fruit extract against sodium valproate-induced postnatal autism in BALB/c mice. Heliyon (2024).
2. Sedation Therapy in Intensive Care Units: Harnessing the Power of Antioxidants to Combat Oxidative Stress. Biomedicines (2023).
3. Oxidative Brain Injury Induced by Amiodarone in Rats: Protective Effect of S‐methyl Methionine Sulfonium Chloride. Acta Chimica Slovenica (2023).