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Evaluating the Effect of Seizure Induction on Top of HFCD and/or Vitamin E Administration on the Levels of Oxidative Stress Biomarkers in the Hippocampus
Author(s) -
Hasan Zuheir A,
Alzoubi Karem H
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.918.5
Subject(s) - oxidative stress , hippocampus , vitamin e , medicine , vitamin c , antioxidant , endocrinology , vitamin , epilepsy , hippocampal formation , neuroprotection , chemistry , biochemistry , psychiatry
There is increasing evidence that oxidative stress is a casual factor in different neurodegenerative disorders such as Alzheimer disease and epilepsy. We have previously shown that consumption of High‐fat high‐carbohydrate diet (HFCD) induces oxidative stress, which results in hippocampal neuronal damage hence impairment of learning and memory, which was reversed by the antioxidant Vitamin E. The reported damage in the hippocampus caused by oxidative stress following consumption of HFCD could alter synaptic transmission in the hippocampus and may increase susceptibility to seizures. Recently, we showed that chronic consumption of HFCD increases, whereas Vitamin E decreases susceptibility to chemically induced seizures using the PTZ seizure threshold model in rats. The present study was undertaken to determine the effect of seizure induction on top of HFCD and/or Vitamin E consumption on the levels of oxidative stress biomarkers in the hippocampus. Male Wistar rats (250–300 gms) were randomly assigned into four groups: control, high‐fat high‐carbohydrate diet (HFCD), vitamin E (Vit E), and high‐fat high‐carbohydrate diet with vitamin E (HFCD + Vit E). Vitamin E and/or HFCD were concurrently administered to animals for 6 weeks. Thereafter, PTZ seizures were induced in half of the animals from each group, whereas the rest of the animals were kept as a control without seizure induction. Thirty minutes later, all animals were killed and hippocampus tissues were extracted for molecular analysis of oxidative stress biomarkers (GSH, GSSG, GSH/GSSG ratio, GPx, SOD, and catalase) using ELISA technique. Results revealed that PTZ seizures were associated with significant increases in oxidative stress biomarkers. These increases were amplified in rats consuming HFCD, whereas they were reduced in rats concurrently administered vitamin E. In rats chronically consuming HFCD and concurrently treated with vitamin E, PTZ seizures induced changes in oxidative stress biomarkers were similar to that in control animals. These data suggest that during the course of PTZ‐induced seizure, prolonged consumption of HFCD increases susceptibility to oxidative stress in the hippocampus. Such an effect is being normalized by concurrent administration of vitamin E. Support or Funding Information Supported by Grants from Jordan University of Science and Technology and Arabian Gulf University