beta-carotene and Epilepsy

To investigate whether epileptic patients who become obese after valproic acid (VPA) therapy can have a high risk of atherosclerosis related to the oxidation of low-density lipoprotein, we prospectively studied the plasma concentrations of lipid-soluble antioxidant vitamins in a group of 20 epileptic girls and 20 controls. After 1 year of VPA treatment, epileptic patients who gained weight had decreased plasma concentrations of alpha-tocopherol and alpha- and beta-carotene, the main lipid-soluble antioxidants. Moreover, 5 patients who gained weight were reevaluated 6 months after withdrawal from VPA therapy and showed normal body mass indices and normalized plasma levels of antioxidants. In conclusion, the data suggest that epileptic patients who gain weight after VPA therapy have reduced plasma concentrations of antioxidant vitamins and that these reductions are reversible after VPA withdrawal.

Topics: Adolescent; alpha-Tocopherol; Anticonvulsants; Antioxidants; beta Carotene; Body Weight; Carotenoids; Child; Epilepsy; Female; Follow-Up Studies; Humans; Obesity; Prospective Studies; Valproic Acid; Weight Gain

It has been widely suggested that oxidative stress products play an important role in the pathophysiology of epilepsy. Capparis ovata (C. ovata) may useful treatment of epilepsy because it contains antioxidant flavonoids. The current study was designed to determine the effects of C. ovata on lipid peroxidation, antioxidant levels and electroencephalography (EEG) records in pentylentetrazol (PTZ)-induced epileptic rats. Thirty-two rats were randomly divided into four groups. First group was used as control although second group was PTZ group. Oral 100 and 200 mg/kg C. ovata were given to rats constituting the third and fourth groups for 7 days before PTZ administration. Second, third and forth groups received 60 mg/kg PTZ for induction of epilepsy. Three hours after administration of PTZ, EEG records, brain cortex and blood samples were taken all groups. The lipid peroxidation levels of the brain cortex, number of spikes and epileptiform discharges of EEG were higher in PTZ group than in control and C. ovata group whereas they were decreased by C. ovata administration. Vitamin A, vitamin C, vitamin E and β-carotene concentrations of brain cortex and latency to first spike of EEG were decreased by the PTZ administration although the brain cortex and plasma vitamin concentrations, and brain cortex and erythrocyte glutathione and glutathione peroxidase values were increased in PTZ + 100 and PTZ + 200 mg C. ovata groups. In conclusion, C. ovata administration caused protection against the PTZ-induced brain oxidative toxicity by inhibiting free radical and epileptic seizures, and supporting antioxidant redox system.

Topics: Animals; Antioxidants; beta Carotene; Brain; Capparis; Cerebral Cortex; Electroencephalography; Epilepsy; Female; Glutathione Peroxidase; Lipid Peroxidation; Pentylenetetrazole; Plant Extracts; Rats; Rats, Wistar; Vitamin A; Vitamin E

It is well known that oxidative stress plays an important role in the etiology of epilepsy. We investigated effects of selenium (Se) and topiramate (TPM) combination supplementation on antioxidant and oxidant values in control and patients with epilepsy and refractory epilepsy. For the aim, we used control (n = 19), epilepsy + TPM (n = 19), epilepsy + TPM + Se (n = 15) groups. We also used control (n = 15), refractory epilepsy (n = 15), and refractory epilepsy + Se (n = 8) groups. TPM (0.2 mg/daily) and Se, as sodium selenite (twice daily with 0.1 mg doses), were orally supplemented to the patients for 45 days. Erythrocyte lipid peroxidation levels were higher in refractory epilepsy groups than in control although its level and seizure numbers were decreased in TPM and TPM + Se supplemented groups of the patients. The erythrocyte reduced glutathione (GSH), glutathione peroxidase (GSH-Px), plasma total antioxidant status (TAS), and vitamin E concentration in refractory epilepsy group were lower than in control. However, the erythrocyte and plasma TAS, erythrocyte GSH and GSH-Px, and plasma vitamins A and C values were increased either by Se or Se + TPM in epilepsy and refractory epilepsy groups. There were no effects of TPM and Se on plasma β-carotene values in the groups. In conclusion, TPM and selenium caused protective effects on the epilepsy and refractory epilepsy-induced oxidative injury by inhibiting free radical production and supporting antioxidant redox system.

Topics: Adult; Antioxidants; Ascorbic Acid; beta Carotene; Case-Control Studies; Epilepsy; Female; Fructose; Glutathione; Glutathione Peroxidase; Humans; Lipid Peroxidation; Male; Oxidative Stress; Pilot Projects; Selenium; Topiramate; Vitamin A; Vitamin E; Young Adult

Vitamin A (Vit A) and its derivatives have recently been reported to be implicated in synaptic plasticity. In this study, the possible effect of Vit A and its precursor, beta-carotene on acute seizure and kindling, induced by pentylenetetrazole (PTZ) was assessed. Vit A and beta-carotene were evaluated for their ability to: (1) elevate the threshold of clonic seizures induced by i.v. infusion of PTZ; (2) suppress the seizures (clonic and tonic) and lethality induced by i.p. PTZ in PTZ-kindled mice (anticonvulsant effect); (3) attenuate the development of sensitization to convulsive and lethal effects of i.p. PTZ in kindled mice (anti-epileptogenic effect). Diazepam was employed as positive control. All the drugs showed anti-epileptogenic effect against PTZ-induced tonic seizures and lethality. Vit A and beta-carotene had no effect on clonic seizures threshold and also on tonic seizures and lethality induced by PTZ in kindled mice. Non-genomic and genomic mechanisms could be involved in the anti-epileptogenic effect of Vit A and beta-carotene.

Topics: Animals; Anticonvulsants; beta Carotene; Disease Models, Animal; Dose-Response Relationship, Drug; Drug Interactions; Epilepsy; Kindling, Neurologic; Male; Mice; Mice, Inbred Strains; Pentylenetetrazole; Seizures; Time Factors; Vitamin A