PubMed · 4460166
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T Zamorano, M Oyarzun. 1974. [Physical capacity for work].. https://pubmed.ncbi.nlm.nih.gov/4460166/
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Using transgenic salt-tolerant wheat 89122 and its receptor Longchun 13 as test material, the dynamic changes of respiration pathway of wheat seedlings at different salt concentration were studied. The appearance of salt respiration was later in 89122 than in Longchun 13. The changes of Valt and rho Valt of both varieties had different patterns during salt stress process. Valt was suppressed by high salt levels, but could be induced by low salt levels in Longchun 13. The rho Valt and rho' Vcyt of two varieties were cooperatively regulated with each other to adapt to salt stress, and rho' Vcyt was the main electron transport pathway. The possible physiological roles of cyanide-resistant respiration were also discussed. It was suggested that the operation intensity of cyanide-resistant respiration could serve as a physiological index of plant salt-tolerance.
As plants are confined to the place where they grow, they have to develop a broad range of defence responses to cope with pathogenic infections. The oxidative burst, a rapid, transient, production of huge amounts of reactive oxygen species (ROS), is one of the earliest observable aspects of a plant's defence strategy. First this Review describes the chemistry of ROS (superoxide radical, hydrogen peroxide and hydroxyl radical). Secondly, the role of ROS in defence responses is demonstrated, and some important issues are considered, such as: (1) which of the ROS is a major building element of the oxidative burst; (2) the spatial and temporal regulation of the oxidative burst; and (3) differences in the plant's responses to biotic and abiotic elicitation. Thirdly, the relationships between the oxidative burst and other plant defence responses are indicated. These include: (1) an oxygen consumption, (2) the production of phytoalexins, (3) systemic acquired resistance, (4) immobilization of plant cell wall proteins, (5) changes in membrane permeability and ion fluxes and (6) a putative role in hypersensitive cell death. Wherever possible, the comparisons with models applicable to animal systems are presented. Finally, the question of the origin of ROS in the oxidative burst is considered, and two major hypotheses, (1) the action of NADPH oxidase system analogous to that of animal phagocytes, and (2) the pH-dependent generation of hydrogen peroxide by a cell wall peroxidase, are presented. On the basis of this material, a third 'unifying' hypothesis is presented, where transient changes in the pH of the cell wall compartment are indicated as a core phenomenon in evoking ROS production. Additionally, a germin/oxalate oxidase system which generates H2O2 in response to pathogenic infection is also described.
An analysis is presented of factors determining the accuracy and spatial resolution of a method for the estimation of oxygen removal rate in tissues using a multi-cathode electrode placed on the tissue surface. The effect of oxygen consumption by the cathodes is shown to be small for 25-micrometer diameter cathodes, but covering the tissue surface with a thin oxygen oxygen-permeable plastic film can introduce a systematic error into the estimate of removal rate, the size of which depends upon the oxygen diffusion coefficient and solubility in the plastic compared with those in the tissue. Spatial resolution is shown to be adequate for distinguishing changes in removal rate over distances of a few hundred microns, and the averaging of removal rate in the direction normal to the tissue surface is weighted heavily towards the superficial tissue layer.