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Gubert C.,Federal University of Rio Grande do Sul | Gubert C.,Instituto Nacional Of Ciencia E Tecnologia Em Medicina Translacional Inct Tm | Stertz L.,Federal University of Rio Grande do Sul | Stertz L.,Instituto Nacional Of Ciencia E Tecnologia Em Medicina Translacional Inct Tm | And 16 more authors.
Journal of Psychiatric Research | Year: 2013

Evidence suggests that mitochondrial dysfunction is involved in the pathophysiology of psychiatric disorders such as schizophrenia (SZ) and bipolar disorder (BD). However, the exact mechanisms underlying this dysfunction are not well understood. Impaired activity of electron transport chain (ETC) complexes has been described in these disorders and may reflect changes in mitochondrial metabolism and oxidative stress markers. The objective of this study was to compare ETC complex activity and protein and lipid oxidation markers in 12 euthymic patients with BD type I, in 18 patients with stable chronic SZ, and in 30 matched healthy volunteers. Activity of complexes I, II, and III was determined by enzyme kinetics of mitochondria isolated from peripheral blood mononuclear cells (PBMCs). Protein oxidation was evaluated using the protein carbonyl content (PCC) method, and lipid peroxidation, the thiobarbituric acid reactive substances (TBARS) assay kit. A significant decrease in complex I activity was observed (p=0.02), as well as an increase in plasma levels of TBARS (p=0.00617) in patients with SZ when compared to matched controls. Conversely, no significant differences were found in complex I activity (p=0.17) or in plasma TBARS levels (p=0.26) in patients with BD vs. matched controls. Our results suggest that mitochondrial complex I dysfunction and oxidative stress play important roles in the pathophysiology of SZ and may be used in potential novel adjunctive therapy for SZ, focusing primarily on cognitive impairment and disorder progression. © 2013 Elsevier Ltd.


Rezin G.T.,University of the Extreme South of Santa Catarina | Rezin G.T.,Instituto Nacional Of Ciencia E Tecnologia Em Medicina Translacional Inct Tm | Scaini G.,University of the Extreme South of Santa Catarina | Scaini G.,Instituto Nacional Of Ciencia E Tecnologia Em Medicina Translacional Inct Tm | And 22 more authors.
Metabolic Brain Disease | Year: 2012

Fenproporex is an amphetamine-based anorectic and it is rapidly converted in vivo into amphetamine. It elevates the levels of extracellular dopamine in the brain. Acetylcholinesterase is a regulatory enzyme which is involved in cholinergic synapses and may indirectly modulate the release of dopamine. Thus, we investigated whether the effects of chronic administration of fenproporex in adult rats alters acquisition and retention of avoidance memory and acetylcholinesterase activity. Adult male Wistar rats received repeated (14 days) intraperitoneal injection of vehicle or fenproporex (6.25, 12.5 or 25 mg/kg i.p.). For behavioral assessment, animals were submitted to inhibitory avoidance (IA) tasks and continuous multiple trials step-down inhibitory avoidance (CMIA). Acetylcholinesterase activity was measured in the prefrontal cortex, hippocampus, hypothalamus and striatum. The administration of fenproporex (6.25, 12.5 and 25 mg/kg) did not induce impairment in short and long-term IA or CMIA retention memory in rats. In addition, longer periods of exposure to fenproporex administration decreased acetylcholinesterase activity in prefrontal cortex and striatum of rats, but no alteration was verified in the hippocampus and hypothalamus. In conclusion, the present study showed that chronic fenproporex administration decreased acetylcholinesterase activity in the rat brain. However, longer periods of exposure to fenproporex did not produce impairment in short and long-termIA or CMIA retention memory in rats. © Springer Science+Business Media, LLC 2012.

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