Lack of association of GPX1 and MnSOD genes with symptom severity and response to clozapine treatment in schizophrenia subjects

Hum Psychopharmacol. 2009 Dec;24(8):676-9. doi: 10.1002/hup.1076.

Abstract

Abnormal activities of critical antioxidant enzymes and other indices of lipid peroxidation in plasma and red blood cells were detected in patients with schizophrenia. Other results have shown that oxidative stress may be modulated by clozapine. Based on that and some studies already found different clinical relations between reactive oxygen species and negative and positive symptoms, we evaluated association between clinical response and the polymorphism in the human glutathione peroxidase (GPX1) (Pro200Leu, rs1050450) and manganese SOD (MNSOD) (Ala16Val, rs4880) gene in 216 clozapine-treated patients with schizophrenia. No association was found with these two functional polymorphisms and clozapine response and symptom change after 6 months. No correlations were found between positive/negative symptoms score and both polymorphisms. Our results present that GPX1 (Pro200Leu) and MNSOD (Ala16Val) polymorphisms seem do not play a central role in the clozapine response, although studies in larger and independent samples are necessary to confirm our findings.

MeSH terms

  • Adult
  • Antipsychotic Agents / pharmacology
  • Antipsychotic Agents / therapeutic use*
  • Clinical Trials as Topic
  • Clozapine / pharmacology
  • Clozapine / therapeutic use*
  • Female
  • Glutathione Peroxidase / genetics
  • Glutathione Peroxidase GPX1
  • Humans
  • Male
  • Polymorphism, Genetic
  • Schizophrenia / drug therapy*
  • Schizophrenia / genetics
  • Schizophrenia / physiopathology
  • Severity of Illness Index
  • Superoxide Dismutase / genetics
  • Young Adult

Substances

  • Antipsychotic Agents
  • Glutathione Peroxidase
  • Superoxide Dismutase
  • Clozapine
  • Glutathione Peroxidase GPX1
  • GPX1 protein, human