In source leaves of resistant tobacco, oxidative burst and subsequent formation of hypersensitive lesions after infection with Phytophthora nicotianae was prevented by inhibition of glucose-6-phosphate dehydrogenase (G6PDH) or NADPH oxidases. This observation indicated that plant defense could benefit from improved NADPH availability due to increased G6PDH activity in the cytosol. A plastidic isoform of the G6PDH-encoding gene, G6PD, displaying high NADPH tolerance was engineered for cytosolic expression (cP2), and introduced into a susceptible cultivar. After infection, transgenic (previously susceptible) lines overexpressing cP2 showed early oxidative bursts, callose deposition, and changes in metabolic parameters. These responses resulted in timely formation of hypersensitive lesions similar to resistant plants, although their extent varied considerably between different transgenic lines. Additional RNAi suppression of endogenous cytosolic G6PD isoforms resulted in highly uniform defense responses and also enhanced drought tolerance and flowering. Cytosolic G6PDH seems to be a crucial factor for the outcome of plant defense responses; thus, representing an important target for modulation of stress resistance. Because isoenzyme replacement of G6PDH in the cytosol was beneficial under various kinds of cues, we propose this strategy as a tool to enhance stress tolerance in general.oxidative burst ͉ source-to-sink transition ͉ NADPH availability ͉ pathogen resistance ͉ tobacco P lants are under continuous threat of being challenged by pathogenic microorganisms, which try to exploit them as a source of carbohydrates and other assimilates. Timely recognition of invading microorganisms and rapid and effective induction of defense responses are presently considered the main difference between pathogen-resistant and susceptible plant lines (1). So-called compatible interactions between pathogens and plants result if the pathogen can overcome plant defense barriers and establish disease symptoms. During an incompatible interaction, a wealth of defense mechanisms [e.g., generation of reactive oxygen species (ROS), synthesis of pathogenesis-related (PR) proteins, cell-wall fortification, and the hypersensitive reaction (HR)] can efficiently limit pathogen growth. The HR, which includes ROS formation and programmed cell death (PCD), represents the most efficient mechanism of plant defense. ROS were previously proposed to orchestrate the establishment of plant defense responses (2, 3). NADPH oxidases at the plasma membrane are considered the main source of extracellular ROS formation during defense, the so-called oxidative burst. Down-regulation or elimination of NADPH oxidase leads to suppression of pathogen-induced oxidative bursts and HR (4).The oxidative burst, an evolutionarily conserved mechanism, is part of the innate immune response, and (besides triggering plant PCD) it is thought to contribute to direct killing of invading microorganisms. It also helps to mount an invasion barrier through radical-mediated polymer...
The polyphenol-rich extract of a consumer-relevant apple juice blend was found to potently inhibit the growth of the human colon cancer cell line HT29 in vitro. The epidermal growth factor receptor (EGFR) and its subsequent signaling cascade play an important role in the regulation of cell proliferation in HT29 cells. The protein tyrosine kinase activity of an EGFR preparation was effectively inhibited by the polyphenol-rich apple juice extract. Treatment of intact cells with this extract resulted in the suppression of the subsequent mitogen-activated protein kinase cascade. Amongst the so far identified apple juice constituents, the proanthocyanidins B1 and B2 as well as quercetin-3-glc (isoquercitrin) and quercetin-3-gal (hyperoside) were found to possess substantial EGFR-inhibitory properties. However, as to be expected from the final concentration of these potential EGFR inhibitors in the original polyphenol-rich extract, a synthetic mixture of the apple juice constituents identified and available so far, including both proanthocyanidins and the quercetin glycosides, showed only marginal inhibitory effects on the EGFR. These results permit the assumption that yet unknown constituents contribute substantially to the potent EGFR-inhibitory properties of polyphenol-rich apple juice extract. In summary, the polyphenol composition of apple juice possesses promising growth-inhibitory properties, affecting proliferation-associated signaling cascades in colon tumor cells.
The aglycons of the most abundant anthocyanins in food, cyanidin (cy) and delphinidin (del), represent potent inhibitors of the epidermal growth factor receptor (EGFR). Structure-activity studies show that the presence of vicinal hydroxy substituents at the phenyl ring at the 2-position (B-ring) is crucial for target interaction. The presence of a single hydroxy group or introduction of methoxy substituents at the B-ring results in a substantial loss of inhibitory properties. However, biological activity is not exclusively limited to compounds bearing vicinal hydroxy groups. A contradictory structure-activity relationship is observed for the inhibition of cAMP-specific phosphodiesterases (PDEs). Of the anthocyanidins tested, malvidin, bearing methoxy substituents in the 3'- and 5'-positions, most effectively inhibited cAMP hydrolysis. The absence of methoxy groups and/or replacement by hydroxy substituents was found to strongly diminish PDE-inhibitory properties. We found that either effective EGFR inhibition or effective PDE inhibition is required to achieve a shut-down of the central mitogen-activated protein kinase (MAPK) pathway, a signaling cascade crucial for the regulation of cell growth. This is consistent with the finding that efficient reduction of cell growth is limited to anthocyanidins that are potent EGFR- or PDE-inhibitors including cy and del or malvidin (mv), respectively. In summary, depending on the substitution pattern at the B-ring, anthocyanidins interfere with different signaling cascades involved in the regulation of cell growth.
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