AI Article Synopsis
- The study investigates the role of free radicals and scavenger enzymes in seizures using a rat model of epilepsy induced by pilocarpine.
- The research found that superoxide dismutase (SOD) activity decreased and hydroperoxide (HPx) levels increased after prolonged seizure activity, indicating oxidative stress.
- The findings suggest that lipid peroxidation during seizure events may lead to neuronal damage in the hippocampus, highlighting the detrimental effects of reactive oxygen species in epilepsy.
Article Abstract
The relationship between free radical and scavenger enzymes has been found in the epileptic phenomena and reactive oxygen species have been implicated in seizure-induced neurodegeneration. Using the epilepsy model obtained by systemic administration of pilocarpine (PILO) in rats, we investigated the superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities as well as the hydroperoxide (HPx) concentration in the hippocampus of rats during status epilepticus (SE), silent and chronic periods. The enzyme activities as well as the HPx concentration were measured using spectrophotometric methods and the results compared to values obtained from saline-treated animals. The SOD activity decreased after long-lasting SE period and during the chronic phase. In addition, HPx levels increased in same periods whereas the GPx activity increased only in the hippocampus of animals submitted to 1 h of SE. Animals presenting partial seizures, those submitted to 5 h of SE and animals from the silent period (seizure free) showed normal levels of SOD, GPx and HPx. These results show a direct evidence of lipid peroxidation during seizure activity that could be responsible for neuronal damage in the hippocampus of rats, during the establishment of PILO model of epilepsy.
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| http://dx.doi.org/10.1016/s0920-1211(01)00269-8 | DOI Listing |
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