Upon infection, a rapid increase of polyphenoloxidase and peroxidase activity was found whenever host-virus combinations resulted in the formation of local lesions. The activation of phenol-oxidizing enzymes was slower and less in systemic hosts. The development of local lesions in Nicotiana glutinosa L. was accompanied by the decrease of o-dihydric phenols, mainly chlorogenic acid, in the host tissues. Histochemical tests suggested that, simultaneously, toxic quinones accumulate in the necrotic area. The production of quinones results in a rapid breakdown of added ascorbic acid in the tissues. Feeding of ascorbic acid or other reducing compounds (cysteine, glutathione) to the tissues in high concentrations markedly inhibited lesion formation, apparently by replacing the consumed endogenous reducing power and holding the phenols in a reduced state, and not by inhibiting the polyphenoloxidases. The development of local symptoms and the multiplication of viruses are not necessarily connected with each other since tobacco mosaic virus (TMV) did multiply in the ascorbic acid-treated N. glutinosa tissues without lesion formation. Around the lesions, in the healthy tissues, dehydrogenases are enormously activated and probably represent a defense reaction that helps to keep the phenolics in a reduced state. The role of polyphenol oxidation in lesion development is also shown by the relatively low activation of polyphenoloxidases in local lesion hosts upon exposure to 36° C, which results in a shift to systemic response.
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