complex i deficiency in persian multiple sclerosis patients

multiple sclerosis (ms) is a demyelinating disease of the central nervous system characterized by morphological hallmarks of inflammation, demyelination and axonal loss. to date, little attention has been paid to the contribution of mitochondrial respiratory chain enzyme activities to ms. in this study, kinetic analysis of mitochondrial respiratory chain complex i enzyme (measured as nadh ferricyanide reductase) was performed on intact mitochondria isolated from fresh skeletal muscle in ms patients (n =10) and control subjects (n =11). mitochondrial dna common deletion and deletions were also tested in ms patients. our findings showed that complex i activities were significantly reduced (p=0.007) in patients compared to controls. however, we could not find any deletion in mtdna in patients with ms. the presupposition of the relationship between ms and mitochondrial disorders is due to the predominant maternal transmission of ms in affected parent–child pairs, pathoaetiological role of respiratory chain dysfunction in multisystem disorders and the important role of it in neurodegenerative disorders, a number of patients such as lhon or other mtdna abnormalities with developed neurological symptoms indistinguishable from ms and similarity of clinical symptoms in mitochondrial disorders to those of ms. this study suggested that a biochemical defect in complex i activity might be involved in the pathogenesis of ms.