INVESTIGADORES
BORRONI Maria Virginia
congresos y reuniones científicas
Título:
Nitric Oxide and Oxidative Stress in Iron Overloaded Rats
Autor/es:
GALLEANO, M; AIMÓ, L; BORRONI, M. V; PUNTARULO, S.
Lugar:
Ventura, California
Reunión:
Simposio; The Third Gordon Reaserch Conference: Nitric Oxide in Biochemistry and Biology; 1999
Institución organizadora:
Gordon Reaserch Conferences
Resumen:
The Third Gordon Reaserch Conference: Nitric Oxide in Bicemistry and Biology February 7-12,1999 Nitric Oxide and Oxidative Stress in Iron Overloaded Rats Galleano, M.; Aimó, L.;.Borroni, M. V and Puntarulo, S. Physical Chemistry-PRALIB, School of Pharmacy and Biochemistry, University of Buenos Aires, Buenos Aires, Argentina The main objective of this work was to study the effect of in vivo iron overload on lipid oxidation and nitric oxide (NO) formation both, with and without administration of bacterial lipopolysacharide (LPS). Male adults Wistar were injected ip with saline solution (Control); iron-dextran 200 mg/Kg (Fe); Escherichia coli lipopolysacharide 4 mg/Kg prepared in saline solution (LPS); and iron-dextran 200 mg/Kg plus LPS 4 mg/Kg simultaneously (Fe+LPS) during 5 h. Diethyldithiocarbamate (DETC) 2.2 mmol/Kg was injected ip.30 min before measurements. Hepatic (DETC)2-Fe-NO complex detected by EPR, and TBARS content are shown in Table 1. Plasmatic content of ascorbyl radical (AR), detected by EPR, and ascorbic acid (AA), assessed by HPLC, were measured. The net increase in the ratio (AR/AA) induced by iron was not significantly affected by LPS administration (1.2±0.3 and 0.9±0.3 for non-LPS and LPS treated groups, respectively). These data suggest that under these experimental conditions the net increase in (DETC)2-Fe-NO detection in liver from iron overloaded rats was significant higher in the presence (7±3 AU) than in the absence of LPS(1.1±0.1). However, liver lipid peroxidation mediated by iron, was lower in LPS injected groups than in non-LPS injected groups, suggesting that NO could be a contributing factor for controlling lipid oxidation.