Evidence that the activities of erythrocyte free radical scavenging enzymes and the products of lipid peroxidation are increased in different forms of schizophrenia

Abstract

In order to examine antioxidant status and lipid peroxidation in schizophrenia patients, activities of three free radical scavenging enzymes (superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT)), and the level of thiobarbituric acid-reactive substances (TBARS) as an index of lipid peroxidation have been studied in red blood cells. Schizophrenic patients were divided into three groups (disorganized (n = 21), paranoid (n = 26) and residual types (n = 18)) to determine differences between subgroups. SOD, CAT and GSH-Px activities in the control group were found to be 1461.0 +/- 248.6 U g(-1) Hb, 148.2 +/- 59.3 k g(-1) Hb and 25.87 +/- 4.25 U g(-1) Hb, respectively. We found no significant differences in SOD activities between study and control groups. There was a significant increase in SOD activity in the residual group compared to the paranoid group (P < 0.005). CAT activity was found to be increased in disorganized (148%), paranoid (147%), and residual (165%) groups compared to the control group. GSH-Px activity was markedly increased in the study groups except the paranoid group. Statistically significant (3-4 fold) increases in TBARS levels of red blood cells were found in all the study groups. It is proposed that antioxidant status may be changed in schizophrenia and thus may induce lipid peroxidation. Therefore, oxidative stress may have a pathophysiological role in all the subtypes of schizophrenia.

Imbalanced free radicals and antioxidant defense systems in schizophrenia: A comparative study

“…High-density polyunsaturated fatty acid (PUFA) is quite sensitive to free radicals. Increased lipid peroxidation reaction occurs and produces more LPO that damages the neuron membranes (Herken et al, 2001a;Yao et al, 2000a); this may explain the increased LPO level in the patient group.…”

“…Superoxide dismutase (SOD), a key enzyme involved in the detoxification of superoxide radicals, has been consistently found increased (Vaiva et al, 1994;Yao et al, 1998b;Zhang et al, 2003a) in drug-free patients or those with TD (tardive dyskinesia) (Yao et al, 1998b;Zhang et al, 2003a), unchanged (Herken et al, 2001a) or decreased (Zhang et al, 2006) (Yao et al, 1998b) while unchanged (Yao et al, 1999) or decreased (Zhang et al, 2006) in chronic patients. Other antioxidant enzyme activity such as catalase (CAT) increased (Herken et al, 2001a) in different form of schizophrenia. And plasma proteins including albumin, uric acid and bilirubin in blood are reported lower in haloperidol-managed (Yao et al, 2000b) and first episode schizophrenic patients (Reddy et al, 2003).…”

“…Animal researches showed that nitric oxide synthase inhibitor can resist this reaction (Bujas-Bobanovic et al, 2000;Wiley, 1998). Excess NO production further leads to changes of neuron structure and function involving neuronal membrane damage (Yao et al, 2000a) and increased indices of lipid peroxidation (Herken et al, 2001a). Antioxidant defense status changes accordingly (Herken et al, 2001a;Yao et al, 1998a).…”

“…Excess NO production further leads to changes of neuron structure and function involving neuronal membrane damage (Yao et al, 2000a) and increased indices of lipid peroxidation (Herken et al, 2001a). Antioxidant defense status changes accordingly (Herken et al, 2001a;Yao et al, 1998a). Superoxide dismutase (SOD), a key enzyme involved in the detoxification of superoxide radicals, has been consistently found increased (Vaiva et al, 1994;Yao et al, 1998b;Zhang et al, 2003a) in drug-free patients or those with TD (tardive dyskinesia) (Yao et al, 1998b;Zhang et al, 2003a), unchanged (Herken et al, 2001a) or decreased (Zhang et al, 2006) (Yao et al, 1998b) while unchanged (Yao et al, 1999) or decreased (Zhang et al, 2006) in chronic patients.…”

N-acetyl Cysteine Treatment Rescues Cognitive Deficits Induced by Mitochondrial Dysfunction in G72/G30 Transgenic Mice

“…Moreover, it was shown that G72 genetic variation obviously modulates both the progressive brain changes that characterize schizophrenia (Hartz et al, 2010) and the reductions in temporal lobe and amygdala gray matter in people suffering from bipolar disorder (Zuliani et al, 2009). Furthermore, there is mounting evidence implicating mitochondrial defects and the resulting oxidative stress in the pathogenesis of schizophrenia (Altar et al, 2005;Herken et al, 2001;Mahadik and Mukherjee, 1996;Marchbanks et al, 2003;Prabakaran et al, 2004). Schizophrenic patients display a number of biomarkers indicative of increased oxidative stress, such as reduced GSH levels (Do et al, 2000), increased malondialdehyde levels (Zhang et al, 2006(Zhang et al, , 2007, and altered antioxidant enzyme activities (Gysin et al, 2007;Zhang et al, 2006).…”