title: Oral Inosine Persistently Elevates Plasma antioxidant capacity in Parkinson's disease.
abstract: BACKGROUND
  Higher serum urate predicts slower progression in PD. The aim of this work was to assess whether oral inosine alters antioxidant capacity of plasma or CSF or urinary markers of oxidative injury in early PD.
  
  
  METHODS
  We assayed plasma and CSF antioxidant capacity by ferric-reducing antioxidant power and measured DNA oxidation adduct 8-hydroxydeoxyguanosine from urine in Safety of URate Elevation in PD, a randomized, placebo-controlled trial of oral inosine assessing safety of elevating serum urate from <6 mg/dL to 6.1-7.0 or 7.1-8.0 mg/dL in patients with early PD.
  
  
  RESULTS
  At 6 months, antioxidant capacity was 29% higher among mild and 43% higher among moderate group participants compared to placebo and correlated with change in serum urate (r = 0.86) and inversely with rate of clinical decline (r = -0.26). CSF antioxidant capacity and urine 8-hydroxydeoxyguanosine did not differ.
  
  
  CONCLUSIONS
  The findings demonstrate a dose-dependent, persistent elevation of plasma antioxidant capacity from oral inosine of potential therapeutic relevance.
authors.affiliation: Department of Neurology, Molecular Neurobiology Lab, Massachusetts General Hospital, Boston, Massachusetts, USA.|Departments of Neurology, Brigham and Women's Hospital, Boston, Massachusetts, USA.|Harvard Medical School, Boston, Massachusetts, USA.
authors.forename: Shamik
authors.initials: S
authors.lastname: Bhattacharyya
authors.affiliation: Department of Neurology, Molecular Neurobiology Lab, Massachusetts General Hospital, Boston, Massachusetts, USA.|Harvard Medical School, Boston, Massachusetts, USA.
authors.forename: Rachit
authors.initials: R
authors.lastname: Bakshi
authors.affiliation: Department of Neurology, Molecular Neurobiology Lab, Massachusetts General Hospital, Boston, Massachusetts, USA.
authors.forename: Robert
authors.initials: R
authors.lastname: Logan
authors.affiliation: Departments of Epidemiology and Nutrition, Harvard School of Public Health, Boston, Massachusetts, USA.|Harvard Medical School, Boston, Massachusetts, USA.
authors.forename: Alberto
authors.initials: A
authors.lastname: Ascherio
authors.affiliation: Department of Medicine, Biostatistics Center, Massachusetts General Hospital, Boston, Massachusetts, USA.|Harvard Medical School, Boston, Massachusetts, USA.
authors.forename: Eric A
authors.initials: EA
authors.lastname: Macklin
authors.affiliation: Department of Neurology, Molecular Neurobiology Lab, Massachusetts General Hospital, Boston, Massachusetts, USA.|Harvard Medical School, Boston, Massachusetts, USA.
authors.forename: Michael A
authors.initials: MA
authors.lastname: Schwarzschild
mesh_terms: D000975:Antioxidants / Q000008:administration & dosage / Q000627:therapeutic use*; D018450:Disease Progression; D005260:Female; D006801:Humans; D007288:Inosine / Q000008:administration & dosage / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress / Q000187:drug effects* / Q000502:physiology; D010300:Parkinson Disease / Q000188:drug therapy*; D016896:Treatment Outcome; D014527:Uric Acid / Q000097:blood
chemical_list: D000975:Antioxidants; D014527:Uric Acid; D007288:Inosine
keywords: Parkinson's disease; antioxidant; inosine; uric acid/urate