PMID- 18398470 OWN - NLM STAT- MEDLINE DCOM- 20080610 LR - 20220311 IS - 1932-6203 (Electronic) IS - 1932-6203 (Linking) VI - 3 IP - 4 DP - 2008 Apr 9 TI - Negative correlation between brain glutathione level and negative symptoms in schizophrenia: a 3T 1H-MRS study. PG - e1944 LID - 10.1371/journal.pone.0001944 [doi] LID - e1944 AB - BACKGROUND: Glutathione (GSH), a major intracellular antioxidant, plays a role in NMDA receptor-mediated neurotransmission, which is involved in the pathophysiology of schizophrenia. In the present study, we aimed to investigate whether GSH levels are altered in the posterior medial frontal cortex of schizophrenic patients. Furthermore, we examined correlations between GSH levels and clinical variables in patients. METHODS AND FINDINGS: Twenty schizophrenia patients and 16 age- and gender-matched normal controls were enrolled to examine the levels of GSH in the posterior medial frontal cortex by using 3T SIGNA EXCITE (1)H-MRS with the spectral editing technique, MEGA-PRESS. Clinical variables of patients were assessed by the Global Assessment of Functioning (GAF), Scale for the Assessment of Negative Symptoms (SANS), Brief Psychiatric Rating Scale (BPRS), Drug-Induced Extra-Pyramidal Symptoms Scale (DIEPSS), and five cognitive performance tests (Word Fluency Test, Stroop Test, Trail Making Test, Wisconsin Card Sorting Test and Digit Span Distractibility Test). Levels of GSH in the posterior medial frontal cortex of schizophrenic patients were not different from those of normal controls. However, we found a significant negative correlation between GSH levels and the severity of negative symptoms (SANS total score and negative symptom subscore on BPRS) in patients. There were no correlations between brain GSH levels and scores on any cognitive performance test except Trail Making Test part A. CONCLUSION: These results suggest that GSH levels in the posterior medial frontal cortex may be related to negative symptoms in schizophrenic patients. Therefore, agents that increase GSH levels in the brain could be potential therapeutic drugs for negative symptoms in schizophrenia. FAU - Matsuzawa, Daisuke AU - Matsuzawa D AD - Department of Psychiatry, Chiba University Graduate School of Medicine, Chiba, Japan. FAU - Obata, Takayuki AU - Obata T FAU - Shirayama, Yukihiko AU - Shirayama Y FAU - Nonaka, Hiroi AU - Nonaka H FAU - Kanazawa, Yoko AU - Kanazawa Y FAU - Yoshitome, Eiji AU - Yoshitome E FAU - Takanashi, Junichi AU - Takanashi J FAU - Matsuda, Tsuyoshi AU - Matsuda T FAU - Shimizu, Eiji AU - Shimizu E FAU - Ikehira, Hiroo AU - Ikehira H FAU - Iyo, Masaomi AU - Iyo M FAU - Hashimoto, Kenji AU - Hashimoto K LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20080409 PL - United States TA - PLoS One JT - PloS one JID - 101285081 RN - 0 (Antioxidants) RN - 0 (Receptors, N-Methyl-D-Aspartate) RN - GAN16C9B8O (Glutathione) SB - IM MH - Adult MH - Antioxidants/metabolism MH - Brain/*metabolism MH - Case-Control Studies MH - Cognition MH - Female MH - Genotype MH - Glutathione/*metabolism MH - Humans MH - Magnetic Resonance Spectroscopy/*methods MH - Male MH - Oxidative Stress MH - Prefrontal Cortex/metabolism MH - Receptors, N-Methyl-D-Aspartate/metabolism MH - Schizophrenia/*metabolism/pathology PMC - PMC2275307 COIS- Competing Interests: The authors have declared that no competing interests exist. EDAT- 2008/04/10 09:00 MHDA- 2008/06/11 09:00 PMCR- 2008/04/09 CRDT- 2008/04/10 09:00 PHST- 2008/02/19 00:00 [received] PHST- 2008/02/27 00:00 [accepted] PHST- 2008/04/10 09:00 [pubmed] PHST- 2008/06/11 09:00 [medline] PHST- 2008/04/10 09:00 [entrez] PHST- 2008/04/09 00:00 [pmc-release] AID - 08-PONE-RA-03685R1 [pii] AID - 10.1371/journal.pone.0001944 [doi] PST - epublish SO - PLoS One. 2008 Apr 9;3(4):e1944. doi: 10.1371/journal.pone.0001944.