Clinical biochemistryAug 27, 2005

Seizures caused by pentylenetetrazol change antioxidant enzyme activities, glutathione, and fat damage levels in rat blood and liver

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Updated Apr 6, 2026

Abstract

Pentylenetetrazol-induced epilepsy in adult Wistar rats resulted in significantly reduced antioxidant enzyme activities and increased markers of oxidative stress.

Erythrocyte activities of Cu,Zn-superoxide dismutase and catalase decreased significantly after a single PTZ treatment.
Levels of reduced glutathione in erythrocytes were significantly lower in the epileptic group compared to controls.
Both erythrocyte and liver tissue levels of thiobarbituric acid-reactive substances were significantly higher in epileptic rats.
Liver tissue showed a significant decrease in Cu,Zn-superoxide dismutase activity and reduced glutathione levels in the epileptic group.
Increased activities of glucose-6-phosphate dehydrogenase and selenium-dependent glutathione peroxidase were observed in the liver of epileptic rats.
These findings indicate enhanced oxidative stress in the liver and erythrocytes of epileptic rats.

Simplified

OBJECTIVES: In order to clarify whether oxidative stress accompanies epilepsy, we examined the effects of pentylenetetrazol (PTZ)-induced epilepsy on the lipid peroxidation and antioxidant enzyme activities in erythrocytes and liver tissues of adult Wistar rats.

MATERIALS AND METHODS: The activities of antioxidative enzymes (glucose-6-phosphate dehydrogenase (G-6-PD)), copper, zinc-superoxide dismutase (Cu,Zn-SOD), catalase (CAT), selenium-dependent glutathione peroxidase (Se-GSH-Px) and the levels of reduced glutathione (GSH) and thiobarbituric acid-reactive substances (TBARS) were measured in erythrocytes and liver tissues of pentylenetetrazol (PTZ)-induced epileptic adult Wistar rats.

RESULTS: Single PTZ treatment in a convulsive dose of 50 mg/kg significantly reduced the erythrocyte Cu,Zn-SOD, CAT enzyme activities and GSH levels compared to controls (P < 0.001, P < 0.001, P < 0.05, respectively). Erythrocyte and liver tissue TBARS levels in the epileptic group were significantly higher than controls (P < 0.0001). There was a significant decrease in liver tissue Cu,Zn-SOD activity and GSH levels in the epileptic group (P < 0.0001), whereas significantly higher activities of G-6-PD and Se-GSH-Px were found in the epileptic group.

CONCLUSIONS: Our results demonstrate a generalized diminished antioxidant activity and increased TBARS level indicating enhanced oxidative stress in the liver and erythrocytes of epileptic rats. Increased oxidative stress in the liver of epileptic rats might be due to the activation of the recently found glutamate receptors in the liver. These findings suggest that the use of antioxidants with antiepileptic drugs and new drugs such as type-5 metabotropic glutamate receptor (mGlu5) antagonist (MPEP) might protect erythrocytes and liver tissue against anoxic damage and oxidative stress.

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Seizures caused by pentylenetetrazol change antioxidant enzyme activities, glutathione, and fat damage levels in rat blood and liver

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