Epilepsy is one of the most common neurologic disorders. The currently available antiepileptic agents do not provide adequate control of the disease in all epileptic patients. The present study was conducted to investigate the role of free radical scavengers e.g., lipoic acid and coenzyme Q10, and the calcium channel blocker, nifedipine, on pentylenetetrazol (PTZ)-induced kindling in rats.
A hundred and sixty male albino rats were used in the current study. Animals were divided into 16 groups, 10 animals each. Kindled group, rats injected with subconvulsive doses of PTZ (30 mg/kg), i.p, three times a week for totals of 13 injections Control group, rats received 13 injections of normal saline. Groups 3 and 4, kindled rats were pretreated with diazepam (0.5 mg/kg, i.p) or phenytoin (50 mg/kg, i.p). Groups 5-10 received lipoic acid (50 mg/kg, 1.p) or coenzyme Q10 (10 mg/kg) alone or in combination with diazepam (0.5 mg/kg, i.p) or phenytoin (50 mg/kg, 1.p). Groups 11-16, kindled animals were pretreated with nifedipine (2 mg/kg, i.p) or nifedipine (10 mg/kg, i.p) alone or in combination with diazepam (0.5 mg/kg, i.p) or phenytoin (50 mg/kg, i.p). The convulsive behavior of the animals was evaluated using Racine-scaling method. Biochemical analysis of lipid peroxides levels, glutatione peroxidase, catalase, and superoxide dismutase activities was conducted for blood of all animals
Both the antioxidants and the calcium channel blocker per se demonstrated some protection against PTZ kindling In addition, lipoic acid potentiated the anticonvulsant effects of diazepam and phenytoin. The biochemical analysis of oxidative stress markers came in line with the anticonvulsant effects of drugs. Lipid peroxides and glutathione peroxidase were most Sensitive, whereas catalase and superoxide dismutase were least sensitive to the effects of drugs.
It is concluded that lipoic acid, coenzyme Q10, and niledipine may have important potentials as adjunct medications with antiepileptic drugs, especially in patients refractory to conventional antiepileptic treatment.