title: Ozone protective effects against PTZ-induced generalized seizures are mediated by reestablishment of cellular redox balance and A1 adenosine receptors.
abstract: OBJECTIVE
  Epilepsy is a common seizure disorder affecting approximately 70 million people worldwide. Mitochondrial dysfunction and antioxidant/prooxidant imbalance are emerging as factors that contribute to epileptogenesis. As medical ozone was able to reestablish cellular redox balance and to maintain the protective effects mediated by A1 receptors (A1Rs), the aim of this work was to study ozone's effects on antioxidant/prooxidant balance and to clarify if A1Rs play a role in ozone's protective actions against pentylenetetrazole (PTZ)-induced convulsions in mice.
  
  
  METHODS
  Influence of ozone's treatments in mice submitted to PTZ-induced seizures was studied. Ozone was administered by rectal insufflation 1 mg/kg (5, 10, 15, 20 treatments), one per day, of 1-1·5 ml at an ozone concentration of 20 μg/ml. Mice received PTZ (90 mg/kg i.p.) 24 hours after the last ozone treatment. Oxygen control groups 26 mg/kg were introduced. Latency to first seizure was determined. Antioxidant/prooxidant balance in brain homogenates was studied. A1 adenosine receptors' effects on ozone's protective actions against seizures were evaluated using 8-cyclopentyl-1,3-dipropylxanthine (DPCPX).
  
  
  RESULTS
  Highest latency was observed when mice received 15 ozone treatments. Oxygen + PTZ group did not achieve protection against neither convulsions nor brain oxidative injury. Fifteen treatments of ozone protected against biomolecules oxidative damage and the antioxidant systems as well. 8-Cyclopentyl-1,3-dipropylxanthine abolished the ozone's protection.
  
  
  CONCLUSIONS
  Ozone therapy increased the latency for the first seizure and the survival percentage. These effects are discussed in point of ozone's capacity to reestablish cellular redox balance, decrease biomolecules damage, and regulate activation of A1 adenosine receptors in PTZ-induced seizures.
authors.forename: Akel
authors.initials: A
authors.lastname: Mallok
authors.forename: Jaqueline Dranguet
authors.initials: JD
authors.lastname: Vaillant
authors.forename: María Teresa Díaz
authors.initials: MT
authors.lastname: Soto
authors.forename: Renate
authors.initials: R
authors.lastname: Viebahn-Hänsler
authors.forename: María de Los Angeles Béquer
authors.initials: Mde L
authors.lastname: Viart
authors.forename: Angela Fraga
authors.initials: AF
authors.lastname: Pérez
authors.forename: Rubens Iván Donoso
authors.initials: RI
authors.lastname: Cedeño
authors.forename: Olga Sonia León
authors.initials: OS
authors.lastname: Fernández
mesh_terms: D058916:Adenosine A1 Receptor Antagonists / Q000494:pharmacology; D000818:Animals; D000927:Anticonvulsants / Q000008:administration & dosage*; D000975:Antioxidants / Q000378:metabolism; D001921:Brain / Q000187:drug effects / Q000378:metabolism; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D016877:Oxidants / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects / Q000502:physiology; D010126:Ozone / Q000008:administration & dosage*; D010433:Pentylenetetrazole; D043682:Receptor, Adenosine A1 / Q000378:metabolism; D012640:Seizures / Q000188:drug therapy* / Q000378:metabolism; D014970:Xanthines / Q000494:pharmacology
chemical_list: D058916:Adenosine A1 Receptor Antagonists; D000927:Anticonvulsants; D000975:Antioxidants; D016877:Oxidants; D043682:Receptor, Adenosine A1; D014970:Xanthines; D010126:Ozone; C051360:1,3-dipropyl-8-cyclopentylxanthine; D010433:Pentylenetetrazole
keywords: Adenosine,; Oxidative stress,; Ozone,; Seizures