Phenytoin-induced glutathione depletion in rat peripheral nerve
| Autor: | Angel Raya, Francisco J. Romero, Juan Gallego, Francisco Bosch-Morell, Joaquín Romá |
|---|---|
| Rok vydání: | 1995 |
| Předmět: |
Male
Phenytoin Antioxidant medicine.medical_treatment Action Potentials In Vitro Techniques Pharmacology medicine.disease_cause Biochemistry Piperazines chemistry.chemical_compound 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine Physiology (medical) polycyclic compounds medicine Animals Enzyme Inhibitors Rats Wistar Muscle Skeletal Evoked Potentials Protein Kinase C Protein kinase C Motor Neurons Analysis of Variance technology industry and agriculture Neurotoxicity Glutathione Isoquinolines medicine.disease Sciatic Nerve Rats Kinetics chemistry Anticonvulsants lipids (amino acids peptides and proteins) Sciatic nerve Oxidative stress Intracellular medicine.drug |
| Zdroj: | Free Radical Biology and Medicine. 19:665-667 |
| ISSN: | 0891-5849 |
| DOI: | 10.1016/0891-5849(95)00031-r |
| Popis: | Administration of high doses (150–250 mg/kg body weight) of phenytoin (DPH) promote a 40% decrease in glutathione (GSH) content of rat sciatic nerve. This DPH-induced GSH depletion is accompanied with an electrophysiological impairment of peripheral neuromuscular function. H7 (20 mg/kg body weight IP, 30 min prior to DPH), a protein kinase C inhibitor, was able to prevent the DPH-induced GSH depletion only at the lower DPH dose used. This same inhibitor completely prevented the electrophysiological impairment at the lower DPH dose, and only partially at the higher DPH dose used. These results confirm the hypothesis of a DPH-dependent activation of PKC (that might be triggered by, or be the consequence of, the reduction of the intracellular antioxidant GSH), as one of the pathophysiological mechanisms involved in DPH-induced neurotoxicity. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Full Text from ScienceDirect