Respiratory-chain enzyme activities in isolated mitochondria of lymphocytes from patients withParkinson′s disease: Preliminary study

Abstract

Evidence suggests that mitochondrial dysfunction stimulates the production of reactive oxygen species (ROS) that promote neural cell death in stroke and in Parkinson's disease. The sites of mitochondrial ROS production are not established but are generally believed to be located within the electron transport chain. We studied the mitochondrial respiratory chain enzymes function from human circulating lymphocytes. Open study. Forty patients with Parkinson's disease (PD) with 30 age-matched control subjects were selected in this study. The patients had received no treatment before the study was conducted. The data from patients and controls were compared using two-tailed student's t-test and values were expressed as means +/- standard deviation (SD). Respiratory complex I + III and IV activities were significantly lower (P < 0.001) in patients than in control subjects. The use of lymphocytes for investigating the respiratory chain enzymes provides an easy, noninvasive method to assess mitochondrial function in patients with PD. Furthermore, our study supports the hypothesis that a biochemical defect in the respiratory chain may be involved in the pathogenesis of PD.