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Seizure‐induced formation of isofurans: novel products of lipid peroxidation whose formation is positively modulated by oxygen tension
Author(s) -
Patel Manisha,
Liang LiPing,
Hou Huagang,
Williams Benjamin B.,
Kmiec Maciej,
Swartz Harold M.,
Fessel Joshua P.,
Roberts L. Jackson
Publication year - 2008
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2007.04974.x
Subject(s) - status epilepticus , chemistry , lipid peroxidation , hippocampal formation , oxygen , oxidative stress , in vivo , biophysics , hypoxia (environmental) , superoxide , epilepsy , endocrinology , biochemistry , neuroscience , biology , microbiology and biotechnology , organic chemistry , enzyme
We have previously shown that seizures induce the formation of F 2 ‐isoprostanes (F 2 ‐IsoPs), one of the most reliable indices of oxidative stress in vivo . Isofurans (IsoFs) are novel products of lipid peroxidation whose formation is favored by high oxygen tensions. In contrast, high oxygen tensions suppress the formation of F 2 ‐IsoPs. The present study determined seizure‐induced formation of IsoFs and its relationship with cellular oxygen levels (pO 2 ). Status epilepticus (SE) resulted in F 2 ‐IsoP and IsoF formation, with overlapping but distinct time courses in hippocampal subregions. IsoF, but not F 2 ‐IsoP formation coincided with mitochondrial oxidative stress. SE resulted in a transient decrease in hippocampal pO 2 measured by in vivo electron paramagnetic resonance oximetry suggesting an early phase of seizure‐induced hypoxia. Seizure‐induced F 2 ‐IsoP formation coincided with the peak hypoxia phase, whereas IsoF formation coincided with the ‘reoxygenation’ phase. These results demonstrate seizure‐induced increase in IsoF formation and its correlation with changes in hippocampal pO 2 and mitochondrial dysfunction.