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Influence of antioxidants on the blood-brain barrier permeability during epileptic seizures

✍ Scribed by Baria Öztaş; Şehri Kılıç; Esen Dural; Turgay İspir

Publisher
John Wiley and Sons
Year
2001
Tongue
English
Weight
94 KB
Volume
66
Category
Article
ISSN
0360-4012

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✦ Synopsis

Abstract

Pentylenetetrazol‐induced seizures in rats lead to the breakdown of the blood‐brain barrier. We compared the disruption of the blood‐brain barrier during epileptic seizure in untreated rats and in rats treated with vitamin E or selenium. The rats were supplemented with nontoxic doses of sodium selenite (4 pp) in drinking water for 3 months, or vitamin E (70 mg/kg) was given intraperitoneally for 30 min before the pentylenetetrazole injection. Evans‐blue was used as a blood‐brain barrier tracer and was given intravenously at a dose of 4 ml/kg of a 2% solution. The rats were divided into four experimental groups. Group I: control (n = 24); Group II: pentylenetetrazole‐induced seizure (n = 12); Group III: vitamin E injected + seizure (n = 12); Group IV: Selenium supplemented + seizure (n = 12). The rats subjected to epileptic seizures showed Evans‐blue albumin extravasations especially in the thalamic nuclei, brainstem, occipital, and frontal cortex. Mean values for Evans‐blue dye were found to be 0.28 ± 0.04 mg % brain tissue in control rats and 1.6 ± 0.2 mg % brain tissue after epileptic seizures (P < 0.01). The magnitude of distribution of the blood‐brain barrier during epileptic seizures was significantly less in rats treated with vitamin E or selenium. The mean value for Evans‐blue dye was found to be 1.2 ± 0.1 mg % brain tissue in selenium supplemented rats and 1.2 ± 0.1 mg % brain tissue in vitamin E injected rats after epileptic seizures. This difference between treated and untreated animals was found to be significant (P < 0.05). The findings of the present study suggest that free radicals contribute to disruption of the blood‐brain barrier during pentylenetetrazol‐induced seizures. J. Neurosci. Res. 66:674–678, 2001. © 2001 Wiley‐Liss, Inc.

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