Colonic Oxidative And Mitochondrial Function In Parkinson’s Disease And Idiopathic REM Sleep Behavior Disorder
C. Morén, Í. González-Casacuberta, J. Navarro-Otano, D. Juárez-Flores, D. Vilas, G. Garrabou, J. C. Milisenda, C. Pont-Sunyer, M. Catalán-García, M. Guitart-Mampel, E. Tobías, F. Cardellach, F. Valldeoriola, A. Iranzo, E. Tolosa
Objective. To determine potential mitochondrial and oxidative alterations in colon biopsies from idiopathic REM sleep behavior disorder (iRBD) and Parkinson’s disease (PD) subjects. Methods. Colonic biopsies from 7 iRBD subjects, 9 subjects with clinically diagnosed PD, and 9 healthy controls were homogenized in 5% w/v mannitol. Citrate synthase (CS) and complex I (CI) were analyzed spectrophotometrically. Oxidative damage was assessed either by lipid peroxidation, through malondialdehyde and hydroxyalkenal content by spectrophotometry, or through antioxidant enzyme levels of superoxide dismutase-2 (SOD2), glutathione peroxidase-1 (Gpx1), and catalase (CAT) by western blot. The presence of mitochondrial DNA (mtDNA) deletions was assessed by long PCR and electrophoresis. Results. Nonsignificant trends to CI decrease in both iRBD (; 23% decrease) and PD patients (; 37% decrease) were found compared to controls (, : NS). Lipid peroxidation was maintained among groups (iRBD: , PD: , and controls: ; : NS). Antioxidant enzymes SOD2 (iRBD: , PD: , and controls: ) and Gpx1 (iRBD , PD: , and controls: ) did not show significant differences between groups. CAT was only detected in 2 controls and 1 iRBD subject. One iRBD patient presented a single mtDNA deletion.