Mitochondrial complex I and IV activities in leukocytes from patients with parkin mutations

MUFTUOGLU M., ELIBOL B., DALMIZRAK O., Ercan A., KULAKSIZ G., OGUS H., ...Daha Fazla

MOVEMENT DISORDERS, cilt.19, sa.5, ss.544-548, 2004 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 19 Sayı: 5
  • Basım Tarihi: 2004
  • Doi Numarası: 10.1002/mds.10695
  • Dergi Adı: MOVEMENT DISORDERS
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.544-548
  • Anahtar Kelimeler: Parkinson's disease, complex I, complex IV, mDNA, ANTIOXIDANT DEFENSES, OXIDATIVE DAMAGE, NITRIC-OXIDE, PLATELETS, GENETICS, DISEASE, PATHOGENESIS, INHIBITION, DEPLETION, PATHWAY
  • Hacettepe Üniversitesi Adresli: Evet

Özet

The parkin protein functions as a RING-type ubiquitin protein ligase. Considering the possibility that impaired ubiquitin-proteosomal system activity may impair antioxidant defenses and enhance oxidative stress, we have investigated the activity of mitochondrial respiratory enzymes in patients with parkin gene mutations. A significant decrease in the leukocyte complex I activity was found both in patients with parkin mutations (62.5%) and idiopathic PD (64.5%) compared with age-matched controls (P < 0.001). Complex IV activity was also decreased significantly in idiopathic PD patients (60%), but no difference was detected between controls and patients with parkin mutations. (C) 2003 Movement Disorder Society.