INVESTIGADORES
PODEROSO Juan Jose
congresos y reuniones científicas
Título:
Increase in nitric oxide release by activated neutrophils in Parkinson's disease.
Autor/es:
GATTO E; CARRERAS MC; PARGAMENT GA; REIDES C; REPETTO M; LLESUY S; FERNÁNDEZ PARDAL M; PODEROSO JJ
Lugar:
Los Angeles, EEUU
Reunión:
Congreso; First International Conference. Biochemistry and Molecular Biology of Nitric Oxide.; 1994
Resumen:
Previous studies reported the presence of oxidative stress in Parkinson’s Disease (PD); increased luminol-dependent chemiluminescence (LDC) by neutrophils (PMN) in these patients has been related to an overproduction of oxygen free radicals. Nitric oxide (NO), now considered as a neuromodulator, is also released by PMNand can interact with reactive oxygen species. The objective to this study was to determine the simultaneous rate of production of NO, hydrogen peroxide (H2O2) and LDC by PMN and other markers of oxidative stress in PD. The diagnosis of PD was made in accord to CAPIT Committee; the study included 9 patients (56±3 ys old, both sex) in II to V Hoehn and Yahr staging. Patients were allowed to stop all medication at 10.00 P; and venous blood samples were taken at 9.00 AM as well as simultaneous samples of healthy donors. No was measured spectrophotometrically by the conversion of oxymyoglobin to metmyoglobin at 592-577 nm. All measurements were done before and after PMN activation with phorbol 12-myristate 13-acetate. Plasmatic antioxidant capacity was stimated with vitamin E analog Trolox and erythrocyte catalase by an standard method. The results showed that NO release was higher in activated PMN from PD than in controls (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 (187.5±21.3 vs 326.4±15.0 U Trolox, p<0.05) as well as catalase levels. The data suggest that, in PD: 1. the simultaneous increase in NO and H2O2 release by PMN could contribute to lipid peroxidation and oxidative stress evidenced by the lowering in antioxidant defences, 2. enhanced LDC could be related to NO-reactive oxygen species interactions and 3. a more generalized defect to explain neurological damage should be discussed.