INVESTIGADORES
PODEROSO Juan Jose
congresos y reuniones científicas
Título:
Nitric oxide in Parkinson’s disease: increase release by activated neutrophils.
Autor/es:
GATTO E; CARRERAS MC; PARGAMENT GA; REIDES C; REPETTO M; LLESUY S; FERNÁNDEZ PARDAL M; PODEROSO JJ
Lugar:
Orlando, EEUU
Reunión:
Congreso; Third International Congress of Movement Disorders; 1994
Resumen:
Oxidative stress have been suggested in the patogénesis of Parkinson’s disease (PD). Recently, Kalra J et al (Mol Cell Biochem 1992; 112:181-186) have reported an increase in luminol-dependent chemiluminescent activity (LDC) in PMN of patients with PD. These results have been related to an overproduction of oxygen free radicals (OFR). Nitric oxide (NO) a novel neuromodulator is also released by PMN and can interact with reactive oxygen species. We therefore studied the simultaneous rate of production of NO, hydrogen peroxide (H2O2) and LDC of PMN in patients with PD, before and after PMN activation; plasmatic antioxidant capacity and erythrocyte catalase were measured as well. Nine patients with idiopathic PD were selected (8 male and 1 female; mean age 56±3), the mean Hoehn Yahr stage when “off” was 3.3 (2 to 5). All medication was stopped at 10 PM and venous blood samples from patients and healthy donors were taken at 9AM. NO release was higher in activated PMN from PD than in control (0.90±0.06 vs 0.65±0.03 nmol/min/106 PMN, p<0.01) as well as H2O2 release (1.12±0.06 vs 0.90±0.06 nmol/min/106 PMN, p<0.05). Plasmatic antioxidant capacity was lower in PD (p<0.05), as well as catalase levels. Our findings may be interpreted as a more generalized defect to explain neurological damage supporting the oxidant stress hypothesis in pathogenesis of PD. Further studies are needed to determine the role of NO in PD.