Lipoic acid alters delta-aminolevulinic dehydratase, glutathione peroxidase and Na+,K+-ATPase activities and glutathione-reduced levels in rat hippocampus after pilocarpine-induced seizures.
In the present study, we investigated the effects of lipoic acid (LA) in the brain oxidative stress caused by pilocarpine-induced seizures in adult rats. Wistar rats were treated with 0.9% saline (i.p., control group), lipoic acid (10 mg/kg, i.p., LA group), pilocarpine (400 mg/kg, i.p., pilocarpine group), and the association of LA (10 mg/kg, i.p.) plus pilocarpine (400 mg/kg, i.p.), 30 min before the administration of LA (LA plus pilocarpine group). After the treatments, all groups were observed for 1 h. The enzyme activities [delta-aminolevulinic dehydratase (delta-ALA-D), glutathione peroxidase (GPx), glutathione reductase (GR), and Na+,K+-ATPase] as well as the glutathione-reduced (GSH) and ascorbic acid (AA) concentrations were measured using spectrophotometric methods, and the results were compared to values obtained from saline and pilocarpine-treated animals. Protective effects of LA were also evaluated on the same parameters. In pilocarpine group, no changes were observed in GPx and GR activities and AA content. Moreover, in the same group, decrease in GSH levels as well as a reduction in delta-ALA-D and Na+,K+-ATPase activities after seizures was observed. In turn, in LA plus pilocarpine group, the appearance of seizures was abolished, and the decreases in delta-ALA-D and Na+,K+-ATPase activities produced by seizures as well as increases in GSH levels and GPx activity were reversed, when compared to the pilocarpine seizing group. The results of the present study demonstrated that preadministration of LA abolished seizure episodes induced by pilocarpine in rat, probably by reducing oxidative stress in rat hippocampus caused by seizures.
de Freitas
Rivelilson Mendes
RM
Laboratory of Physiology and Pharmacology of Federal University of Piauí, Rua Cícero Eduardo, s/n, Junco, Picos, Piauí, 64600-000, Brazil. rivelilson@ufpi.br
D000818:Animals; D000975:Antioxidants / Q000494:pharmacology / Q000627:therapeutic use; D003292:Convulsants / Q000037:antagonists & inhibitors / Q000633:toxicity; D004195:Disease Models, Animal; D015536:Down-Regulation / Q000187:drug effects / Q000502:physiology; D004798:Enzymes / Q000187:drug effects* / Q000378:metabolism; D005978:Glutathione / Q000187:drug effects* / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000187:drug effects / Q000378:metabolism; D008297:Male; D018696:Neuroprotective Agents / Q000494:pharmacology / Q000627:therapeutic use; D018384:Oxidative Stress / Q000187:drug effects* / Q000502:physiology; D010862:Pilocarpine / Q000037:antagonists & inhibitors / Q000633:toxicity; D000623:Porphobilinogen Synthase / Q000187:drug effects / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D012640:Seizures / Q000188:drug therapy* / Q000201:enzymology* / Q000503:physiopathology; D000254:Sodium-Potassium-Exchanging ATPase / Q000187:drug effects / Q000378:metabolism; D013053:Spectrophotometry / Q000379:methods; D008063:Thioctic Acid / Q000494:pharmacology* / Q000627:therapeutic use
D000975:Antioxidants; D003292:Convulsants; D004798:Enzymes; D018696:Neuroprotective Agents; D010862:Pilocarpine; D008063:Thioctic Acid; D005979:Glutathione Peroxidase; D000623:Porphobilinogen Synthase; D000254:Sodium-Potassium-Exchanging ATPase; D005978:Glutathione