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Seizures oxidative injury

VIII. ANTICHOLINESTERASE-INDUCED SEIZURES, OXIDATIVE INJURY,... [Pg.639]

X. SUPPRESSION OF SEIZURE-INDUCED OXIDATIVE INJURY AND NEURODEGENERATION... [Pg.642]

Oxidative stress e Injury e Ischemia e Seizures e Neurodegenerative diseases... [Pg.478]

In conclusion, the data demonstrated that synergistic mechanisms of cellular disruption caused by anticholinesterase agents led to cellular dysfunction and neurodegeneration. It has also been demonstrated that preventing CF-induced neuronal hyperactivity by pretreatment with MEM and atropine blocks pathways associated with oxidative damage in rat brain. The documented abihty of MEM therapy to reduce free radical generation and lipid peroxidation, prevent HEPs and attenuate the morphological injury provides further support for the role of ROS and RNS in anticholinesterase-induced seizures. [Pg.645]

However, the actual role of ERKl/2 seems to be dependent on various parameters since inhibition of ERKl/2 activation during focal ischemia [41], oxidative stress [42], and a model for hippocampal seizures [43] attenuated neuronal death and cellular injury, indicating a proapoptotic role for ERKl/2. In addition, the inhibition of ERKl/2 activation has been demonstrated to protect a mouse neuronal cell line and rat primary cortical neurons from oxidative stress-induced neurotoxicity [44]. [Pg.246]

See other pages where Seizures oxidative injury is mentioned: [Pg.642]    [Pg.718]    [Pg.825]    [Pg.577]    [Pg.93]    [Pg.169]    [Pg.289]    [Pg.825]    [Pg.639]    [Pg.640]    [Pg.644]    [Pg.683]    [Pg.637]    [Pg.78]    [Pg.511]    [Pg.526]    [Pg.494]    [Pg.243]    [Pg.713]    [Pg.714]    [Pg.716]    [Pg.719]   
See also in sourсe #XX -- [ Pg.639 ]



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