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Oxidative burst injury

From the previously discussed studies, the oxidative burst response appears to integrate and/or orchestrate several defense responses. These provide an adaptive mechanism to counteract attacks on or injury to algal cells and thalli. As shown in Fig. 12.2, the occurrence of an oxidative burst associated with the perception of cell-free extracts of A. operculata was shown to play a crucial role in the natural resistance of C. crispus gametophytes (Bouarab et al. 1999). [Pg.259]

This explanation of an oxidative burst can not be accepted without some reservation first we have to ask, what are the reasons for the increase in the release of superoxide anions from mitochondria after injury The first contact of a pathogen with a cell occurs at the cell wall and does not primarily influence the mitochondria. Second healthy plant cells do not contain free iron ions [114,115] and third free radicals should always generate racemic product mixtures of lipidhydroperoxides (see later) which are often not observed. Moreover the oxidative burst reaction consists of 2 phases, a rather fast but weak one, observed minutes after inoculation with a pathogen and a second large one, 3-6 hours later [75,83]. What causes these two phases [it will be recognized later that the first oxidative burst might not correspond to release of H2O2 but to release of a lipidhydroperoxide (LOOK)]. [Pg.65]


See other pages where Oxidative burst injury is mentioned: [Pg.14]    [Pg.917]    [Pg.313]    [Pg.257]    [Pg.185]    [Pg.918]    [Pg.1]    [Pg.60]    [Pg.60]    [Pg.204]    [Pg.653]    [Pg.552]    [Pg.194]    [Pg.64]    [Pg.64]    [Pg.1793]    [Pg.751]    [Pg.82]    [Pg.323]    [Pg.23]    [Pg.183]    [Pg.458]    [Pg.387]   
See also in sourсe #XX -- [ Pg.557 ]




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