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J Biol Chem, Vol. 274, Issue 51, 36446-36455, December 17, 1999
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From the Lipid peroxidation was investigated in relation
with the hypersensitive reaction in cryptogein-elicited tobacco leaves.
A massive production of free polyunsaturated fatty acid (PUFA)
hydroperoxides dependent on a 9-lipoxygenase (LOX) activity was
characterized during the development of leaf necrosis. The process
occurred after a lag phase of 12 h, was accompanied by the
concomitant increase of 9-LOX activity, and preceded by a transient
accumulation of LOX transcripts. Free radical-mediated lipid
peroxidation represented 10% of the process. Inhibition and activation
of the LOX pathway was shown to inhibit or to activate cell death, and
evidence was provided that fatty acid hydroperoxides are able to mimic
leaf necrotic symptoms. Within 24 h, about 50% of leaf PUFAs were
consumed, chloroplast lipids being the major source of PUFAs. The
results minimize the direct participation of active oxygen species from the oxidative burst in membrane lipid peroxidation. They suggest, furthermore, the involvement of lipase activity to provide the free
PUFA substrates for LOX. The LOX-dependent peroxidative
pathway, responsible for tissue necrosis, appears as being one of the
features of hypersensitive programmed cell death.
CEA-Cadarache, Direction des Sciences du
Vivant, Département d'Ecophysiologie Végétale et de
Microbiologie, Laboratoire de Radiobiologie Végétale,
13108 Saint-Paul Lez Durance Cedex, § Laboratoire de
Biogénèse Membranaire, CNRS, UMR 5544, Université
Victor Ségalan Bordeaux II, 146 Rue Léo Saignant,
33076 Bordeaux Cedex, and ¶ Unité Associée
INRA-Université de Bourgogne 692, Laboratoire de Phytopharmacie
et Biochimie des Interactions Cellulaires,
BV 1540, Dijon Cedex, France
To whom correspondence should be addressed: CEA, Laboratoire
de Radiobiologie Végétale, Dépt. d'Ecophysiologie
Végétale et de Microbiologie, Centre d'Etudes de
Cadarache, 13108 Saint-Paul Lez Durance Cedex, France. Tel.: 33 (0)4 42 25 64 86; Fax: 33 (0)4 42 25 62 86; E-mail:
ctriantaphylid@cea.fr.
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