{Diphenyl diselenide and diphenyl ditelluride increase the latency for 4-aminopyridine-induced chemical seizure and prevent death in mice}

Citation:
Brito, VB, Rocha JBT, Folmer V, Erthal F.  2009.  {Diphenyl diselenide and diphenyl ditelluride increase the latency for 4-aminopyridine-induced chemical seizure and prevent death in mice}. Acta Biochimica Polonica. 56, Number 1

Abstract:

In this work was investigated the effect of pre-treatment with (PhSe) 2 and (PhTe) 2 on chemical seizure and 4-aminopyridine-induced lethality in mice. Additionally, lipid peroxidation levels of whole brain after treatment with 4-aminopyridine and effect of pre-treatment with (PhSe) 2 and (PhTe) 2 on these levels were investigated. Mice were pre-treated with (PhSe) 2 or (PhTe) 2 (50, 100, or 150 $μ$mol/kg) 30 min before 4-aminopyridine (12 mg/kg) administration. The treatment with 4-aminopyridine caused a significant incidence of seizures (clonic, tonic) and death. Pre-treatment with (PhSe) 2 and (PhTe) 2 significantly increased the latency for clonic and tonic seizures, and prevented 4-aminopyridine-induced death. Significantly, the pre-treatment with (PhSe) 2 or (PhTe) 2 increased the latency for clonic seizures in a dose-dependent manner. Additionally, a significant increase was observed in the brain lipid peroxidation level after treatment with 4-aminopyridine, which was significantly inhibited by pre-treatment with 150 $μ$mol/kg (PhSe) 2 or (PhTe) 2 . These results demonstrate that (PhSe) 2 and (PhTe) 2 counteract the harmful effects of 4-aminopyridine. It is possible that this effect results from modulation of the redox state of N-methyl-d-aspartate receptors and/or of Ca 2+ channel activity with subsequent alteration in neurotransmitter release. Importantly, this study provides evidence for anticonvulsant and antioxidant properties of (PhSe) 2 and (PhTe) 2′ which indicates a neuroprotective activity of these compounds.

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