Effects of deferoxamine and a diet deficient in Vitamin E on isoelectric electroencephalographic responses associated with ischemia by the four vessel occlusion method

• Published in: Life sciences (1973) Vol. 57; no. 10; pp. 989 - 996
• Main Authors: Lin, Xue Mei, Waller, Steven B., Dietz, Nancy J.
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier Inc 1995
• Subjects: Animals; Brain - drug effects; Brain - metabolism; Brain - physiopathology; cerebral ischemia; deferoxamine; Deferoxamine - pharmacology; Diet; electroencephalogram; Electroencephalography - drug effects; Ischemic Attack, Transient - physiopathology; Male; Rats; Rats, Sprague-Dawley; Thiobarbituric Acid Reactive Substances - metabolism; vitamin E deficiency; Vitamin E Deficiency - physiopathology; deferoxamine; vitamin E deficiency; cerebral ischemia; electroencephalogram
• ISSN: 0024-3205; 1879-0631
• DOI: 10.1016/0024-3205(95)02034-G

This study reports the effects of subchronic administration of the iron chelator deferoxamine (4.2 mg/day by osmotic minipump for 6 days) and a diet deficient in Vitamin E (15% RDA for 60 days) on the isoelectric electroencephalographic responses associated with 15 minutes of global transient cerebral ischemia in rats. Brain levels of thiobarbiturate-reacting substance (TEARS), a measure of lipid peroxidation, were lower in deferoxamine-treated animals and higher in Vitamin E deficit animals suggesting the treatments altered free radical activity at the time of ischemia. During ischemia, all test animals were observed to lose the righting reflex and enter a quiescent state. Fifty percent of the animals in two control groups (N = 15 per group) demonstrated an isoelectric electroencephalographic pattern (defined as 10% or less of pre-ischemia total EEG power) with a mean onset of 5.44 minutes. One third of the animals treated with deferoxamine (N = 15) experienced an isoelectric encephalogram with a mean onset of 8.6 minutes and 73% of the Vitamin E-deficient group (N = 15) experienced an isoelectric EEG with a mean onset of 3.43 minutes. Following reperfusion, EEG patterns returned to power levels within 20% of pre-ischemia levels in all animals. Control animals obtained this EEG power level within 1.34 minutes, deferoxamine-treated animals within 1.25 minutes and animals provided a diet deficient in Vitamin E within 5.03 minutes. Compared to mean total EEG power prior to the onset of ischemia, mean total EEG power five days after reperfusion was reduced 14% in the control groups and 59% in the Vitamin E-deficient group and increased 123% in the deferoxamine group. Results are discussed in relation to the possible involvement of free radicals in the ischemic and postischemic process.