Santos-Lobato, Bruno L.
Pinheiro, Lucas Cesar
Batalhao, Marcelo E.
Pimentel, Angela V.
Del-Bel, Elaine A.
Número total de Autores: 8
Afiliação do(s) autor(es):
 Univ Sao Paulo, Ribeirao Preto Med Sch, Dept Neurosci & Behav Sci, Ave Bandeirantes 3900, BR-14049900 Ribeirao Preto, SP - Brazil
 Fed Univ Para, Expt Neuropathol Lab, Belem, Para - Brazil
 Univ Sao Paulo, Fac Odontol Ribeirao Preto, Dept Basic & Oral Biol, Ribeirao Preto, SP - Brazil
 Univ Sao Paulo, Nursing Sch Ribeirao Preto, Ribeirao Preto, SP - Brazil
Número total de Afiliações: 4
Tipo de documento:
JOURNAL OF NEURAL TRANSMISSION;
Citações Web of Science:
Levodopa-induced dyskinesia (LID) is a common complication of Parkinson's disease (PD) therapy. Nitric oxide in the central nervous system may have a role in its pathophysiology. The present work investigates plasma and CSF levels of nitric oxide metabolites nitrite and nitrate in patients with PD, LID, and healthy control. We measured plasma and CSF nitrite and nitrate levels in patients with PD with and without LID and in healthy controls. The levels of plasma and CSF nitrite and nitrate were measured by ozone-based chemiluminescence. Sixty-seven participants were enrolled. CSF nitrite levels in patients with PD and LID were higher than in patients with PD without LID and healthy controls. CSF/plasma ratio of nitrite was higher in patients with PD and LID than in patients with PD without LID. The CSF/plasma ratio of nitrite in patients with PD and LID was higher than 1, indicating an intrathecal production of NO in patients with this motor complication. There was an increase in nitrate levels of CSF and CSF/plasma ratio of nitrate in patients with PD and LID compared to the healthy controls. Sex, age at evaluation, disease duration, and levodopa equivalent daily doses, as well as processing and storage time, did not critically influence these results. The present study demonstrated an increase in nitrite and nitrate levels in the central nervous system of patients with PD and LID. This finding strengthens the role of NO on LID pathophysiology. (AU)