Brief report Evidence for oxidative stress in the frontal cortex in patients with recurrent depressive disorder—a postmortem study Tanja Maria Michel a,b, ⁎ , Sophia Frangou b , Dorothea Thiemeyer a , Sibylle Camara a , Julia Jecel a , Keinosuke Nara a,c , Andreas Brunklaus d , Robert Zoechling e , Peter Riederer a a Clinical Neurochemistry, Department Psychiatry and Psychotherapy, University Hospital Würzburg, Fürchsleinstr. 15, 97080 Würzburg, Germany b Section of Neurobiology of Psychosis, Institute of Psychiatry, De Crespigny Park, London, SE 5 8AF, UK c Department of Pharmacology School of Medicine, Showa University Tokyo 142-8555, Japan d Department Paediatrics, Guy's and St. Thomas' Hospital, London SE1 7EP, UK e Department Psychiatry, Hospital Mostviertel Amstetten-Mauer, A 3362 Mauer/Amstetten, Austria Received 10 November 2005; received in revised form 21 February 2006; accepted 20 April 2006 Abstract Prefrontal cortical (PFC) and hippocampal (HI) volume reductions have been consistently found in patients with recurrent depressive disorder (DD). Here we examine the possibility that oxidative stress, widely implicated in neuronal cell damage, may contribute to these brain structural changes. We compared manganese (Mn) and copper/zinc (Cu/Zn) superoxide dismutase (SOD) coenzyme concentrations in postmortem PFC and hippocampal brain tissue from 7 patients with DD and 7 neuropsychiatrically healthy controls using sandwich-type enzyme-linked immunosorbent assay (ELISA) technique. The concentration of Cu/Zn-SOD was significantly increased in the PFC but not in the hippocampus of patients. There was no significant change in Mn-SOD enzyme concentration in either region. Our findings contribute to the growing body of evidence implicating oxidative stress in the pathophysiology of depressive disorder. © 2006 Elsevier Ireland Ltd. All rights reserved. Keywords: Superoxide dismutase; Free radicals; Brain; Antioxidants; Mood disorder; Depression; Hippocampus 1. Introduction Recurrent depressive disorder (DD) (International Statistical Classification of Diseases and Related Health Problems, 10th revision, ICD 10; WHO, 1992) has a lifetime prevalence of about 16% (Doris et al., 1999). It has been estimated that by the year 2020 DD will be the second most significant contributor to global health impairment (Murray and Lopez, 1997). Structural brain imaging studies of patients with DD have consistently reported volumetric reductions in the prefrontal cortex (PFC) and the hippocampus (Campbell et al., 2004). Postmortem studies have revealed striking reductions in glial cell number and density in these brain regions as well as more subtle changes in neuronal Psychiatry Research 151 (2007) 145 – 150 www.elsevier.com/locate/psychres ⁎ Corresponding author. Section of Neurobiology of Psychosis, Institute of Psychiatry, De Crespigny Park, London, SE5 8AF, UK. Tel./fax: +44 207 8480 903. E-mail address: T.Michel@iop.kcl.ac.uk (T.M. Michel). 0165-1781/$ - see front matter © 2006 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.psychres.2006.04.013