INVESTIGADORES
RUIZ oscar Adolfo
artículos
Título:
Do polyamines levels modulate the Lotus glaber NADPH oxidation activity induced by the herbicide methyl viologen?
Autor/es:
JUAN CRUZ CUEVAS, DIEGO H. SÁNCHEZ, MARÍA MARINA & OSCAR A. RUIZ
Revista:
AUSTRALIAN JOURNAL OF PLANT PHYSIOLOGY
Referencias:
Año: 2004 vol. 31 p. 921 - 928
ISSN:
0310-7841
Resumen:
In recent years, there has been a growing interest in NAD(P)H-oxidases responsible for the active generation of reactive oxygen species, due to their role in oxidative burst, signaling and oxidative damage derived from biotic and abiotic stresses. Interestingly, it is reported that NAD(P)H oxidase activity is enhanced in some environmental cues, as zinc deficiency and chilling stress, where zinc and polyamines have been suggested to be involved in the modulation of reactive oxygen species generation. In order to further characterize NAD(P)H oxidation activity during oxidative stress, we exposed Lotus glaber (narrow-leaf trefoil; syn L. tenuis var. Miller) plants to the herbicide methyl viologen and evaluated zinc and polyamines as oxidative stress regulatory compounds. For this purpose, we carried out in-vitro and in-vivo experiments, observing that zinc and “higher” polyamines spermidine and spermine inhibited NAD(P)H oxidase activity and prevented methyl viologen-induced superoxide production. It is suggested that these substances act through a direct effect on flavin oxidases. However, it was not possible to correlate L. glaber free polyamine content with their hypothetical inhibitory role during oxidative stress, probably due to its naturally tolerance to the herbicide. Therefore, a more sensitive species like tobacco was tested. High concentration of methyl viologen induced an increase of free polyamine levels in crude extracts and intercellular fluids. However, only free polyamine content in the intercellular fluids was increased in plants treated with low methyl viologen concentrations. These results supports the notion that polyamine metabolism is involved in the physiological response to oxidative stress.