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Plazma Burst 2 ((BETTER)) Download 97

Although the primary oxidative burst following pathogen recognition occurs in the apoplast, ROS produced in other cellular compartments may also have functions in defense. High levels of ROS can be produced inside the plant cell as by-products of metabolic processes, in particular, light-driven production of ROS as a by-product of photosynthesis (Karpinski et al., 2003; Apel and Hirt, 2004). Uncoupling, or inhibition, of the photosystem machinery in the chloroplast and photorespiration associated with chloroplast and peroxisome function can lead to the formation of high levels of ROS that can dramatically affect cellular homeostasis. It is important to recall the nearly ubiquitous requirement for light in the HR (Goodman and Novacky, 1994), as illustrated by the requirement of high-intensity light for cell death mediated by resistance gene proteins (Tang et al., 1998). Under high-light conditions, photorespiratory ROS mediate different mechanisms of lipid peroxidation leading to cell death than in the dark, underscoring the importance of light during the HR (Montillet et al., 2005).

plazma burst 2 download 97


ROS were proposed to orchestrate the establishment of plant defense response and HR following successful pathogen recognition (Apostol et al., 1989; Levine et al., 1994). Genetic proof for NADPH oxidase-Rboh function in the pathogen-induced oxidative burst came from the analysis of rboh mutants and antisense lines (Simon-Plas et al., 2002; Torres et al., 2002; Yoshioka et al., 2003). Down-regulation or elimination of Rboh leads to elimination of extracellular peroxide formation. Yet, this lack of ROS has variable effects on pathogen growth and HR. For example, a double mutant of the Arabidopsis atrbohD and atrbohF genes displays reduced HR in response to avirulent bacteria (Torres et al., 2002). Similarly, Nbrboh-silenced Nicotiana benthamiana plants are more susceptible to avirulent oomycete Phytophthora infestans, and HR is suppressed (Yoshioka et al., 2003). By contrast, the Arabidopsis atrbohF mutant is more resistant to a weakly virulent strain of the oomycete Hyaloperonospora parasitica and actually displays enhanced HR (Torres et al., 2002). There is also evidence of functional overlap between different Rboh proteins. For example, in Arabidopsis, various phenotypes of the individual atrbohD and atrbohF mutants are accentuated in the double mutant atrbohD atrbohF (Torres et al., 2002; Kwak et al., 2003). Thus, while the Rboh proteins are required for ROS production following successful pathogen recognition, these ROS may serve diverse signaling functions in disease resistance and HR.

Major differences among species were also observed in gain-of-function experiments. While similar durations and intensities of all four elicitor-stimulated ion fluxes appear to be required to activate the oxidative burst, defense gene transcription and phytoalexin synthesis in parsley in the absence of elicitor, the Ca2+ ionophore A23187 alone stimulated phytoalexin accumulation in soybean (42) and carrot cells (44). In tobacco cells, A23187 mimicked elicitor-stimulated Ca2+ fluxes and medium alkalinization but did not induce phytoalexin production (19). A common prerequisite in all of these experimental systems is the elicitor-stimulated activation of Ca2+ influx for initiation of all subsequent defense reactions. In some systems, these Ca2+ fluxes across the plasma membrane are apparently sufficient, whereas in others additional ion channels and pumps seem to be required for the induction of downstream effects. Plasma membrane-located ion channels have also been identified as important components of signal transduction cascades in plant responses to various other environmental and hormonal signals (45). In this context it is interesting to note that different sets of genes are transcriptionally activated in parsley cells upon variation of the nature, duration, and intensity of ion fluxes, possibly indicating a simple means of specifically converting many different external signals into appropriate gene expression patterns by modulating the activities of a comparatively small number of ion channels.

The oxidative burst, the rapid production of O2- and H2O2 by plant cells in response to pathogens and Stressors, is a critical step in plant disease resistance and is controlled by several different elicitor-initiated signaling pathways. While different defense elicitors appear to activate disparate initial steps in signaling the oxidative burst, all of the elicitors tested thus far appear to stimulate pathways that converge on the same three core signaling intermediates: 1) the Ca2+-independent activation of a mitogen-activated protein kinase (MAPK) family member, 2) the influx of Ca2+ into the cytosol, deriving most critically from an internal compartment, and 3) the Ca2+-dependent activation of additional protein kinases including a second MAPK homologue and possibly calcium dependent protein kinases (CDPKs). Data from several recent reports are summarized to place these signaling events into a complete and updated model of signaling to the plant oxidative burst.

Wiles et al. [69] examined the effect of 3 g of coffee, which contained approximately 150-200 mg of caffeine, on treadmill running time. This form and dose was used to mimic the real life habits of an athlete prior to competition. Subjects performed a 1500-m treadmill time trial. Ten subjects with a VO2max of 63.9-88.1 ml/kg/min also completed a second protocol designed to simulate a "finishing burst" of approximately 400 m. In addition, six subjects also completed a third protocol to investigate the effect of caffeinated coffee on sustained high-intensity exercise. Results indicated a 4.2 s faster run time for the caffeinated coffee treatment, as compared to decaffeinated coffee. For the "final burst" simulation, all 10 subjects achieved significantly faster run speeds following ingestion of caffeinated coffee. Finally, during the sustained high-intensity effort, eight of ten subjects had increased VO2 values [69].

It is evident that caffeine supplementation provides an ergogenic response for sustained aerobic efforts in moderate-to-highly trained endurance athletes. The research is more varied, however, when pertaining to bursts of high-intensity maximal efforts. Collomp et al. [46] reported results for a group of untrained subjects, who participated in only 2-3 hours per week of non-specific sport activity. In a fasted state, and in a crossover design, subjects consumed caffeine at a dose of 5 mg/kg as well as a placebo condition, and performed a 30-second Wingate test. Compared to a placebo, caffeine did not result in any significant increase in performance for peak power or total work performed [46]. These results are in agreement with Greer and colleagues [45], where in addition to a lack of performance enhancement with caffeine supplementation (6 mg/kg), subjects classified as non-trained experienced a decline in power, as compared to placebo, during the last two of four Wingate bouts [45]. As previously stated, Crowe et al. [47] reported significantly slower times to reach peak power in the second of two bouts of 60-s maximal cycling. Subjects in that study were untrained in a specific sport and consumed caffeine at a dose of 6 mg/kg [47]. Finally, Lorino et al. [47] examined the effects of caffeine at 6 mg/kg on athletic agility and the Wingate test. Results were conclusive in that non-trained males did not significantly perform better for either the pro-agility run or 30-s Wingate test [73]. In contrast, a study published by Woolf et al. [30] demonstrated that participants who were conditioned athletes achieved greater peak power during the Wingate after consuming caffeine at a moderate dose of 5 mg/kg [30]. It is exceedingly apparent that caffeine is not effective for non-trained individuals participating in high-intensity exercise. This may be due to the high variability in performance that is typical for untrained subjects.


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