Interveinal necrosis

Other cyclic tetrapeptides have also been isolated by Japanese workers and AM toxins I, II, and III, isolated from Alternaria mail., are extremely toxic to certain plant species (9.10). These are constructed of L- i-hydroxyisovaleric acid, L-alanine, c-amino-acrylic acid and, in AM toxin I, L-6(-amino- -( .-methoxyphenyl)-valeric acid. The phenyl residue in AM toxin II is L-t(-amino-S-phenylvaleric acid, while in AM toxin III, it is L-ol-amino-( .-hydroxyphenyl)valeric acid (Figure 2), All the AM toxins produce leaf spot, or necrosis, in apple but as might he expected slight change in substitution (R-group) on the phenyl ring radically alters the specific activity of the molecule. Both AM toxin I and III induce interveinal necrosis in the "Indo" apple cultivar, which is also highly susceptible to A. mail. at concentrations as low as 0.1 pph within 18 h after treatment. In contrast, the resistant apple cultivar "Jonathan" is only affected by 1 ppm of AM toxin I and 10 ppm of AM toxin III. 

Preliminary investigations of plant responses to longer term, lower concentration exposures indicate that symptoms associated with acute and chronic exposure may be quite different. Pinto bean exposed tc submicron sulfuric acid aerosol at concentrations of 1-5 mg/m for periods of several days developed a bifacial, interveinal necrosis very similar to that caused by sulfur dioxide. 

III so that within 18 h of application of 0.1 ppb interveinal necrosis develops. In contrast, the resistant apple variety Jonathan requires 1 ppm of AM toxin I, and 10 ppm of AM toxin III to induce identical responses. If, in the case of AM toxins I and III, only 0.1 ppb produces a response when applied exogenously to apple leaves it is inferred that less than 0.1 ppb reaches the active site and the amount of material necessary for necrotic induction is far less. In addition, fragments of the peptide have, apparently, not been tested for biological activity. 

Are there any changes in colour of leaves or needles Can there be seen signs of necrosis If so, are they irregularly distributed, which often is considered as typical for ozone injury, for example, in tobacco or pinto beans (Plate 7 and 8) Or are they concentrated on leaf margins and tips, which often is observed after the slow accumulation of chloride (Halbwachs, 1963) or fluoride (Guderian et al., 1969) Plate 9 shows typical marginal necrosis of an elm leaf, plate 10 tip necrosis of tulip leaves, whereas the flowers themselves are not injured. Acute injury by SO2 often appears as interveinal chlorosis followed by necrosis which can be seen at an elm leaf in plate 11. On the contrary, ozone injury mostly consists of small chlorotic or necrotic spots. Pine needles (plate 12) and... 

The first and fairly obvious point to be made is that acute effects, e.g. plant death, necrosis, collapsed interveinal areas of broad leaves, loss of pine needles, are easiest to detect and therefore more is understood of the mechanisms involved. Most of the established cases of acute SO2 effects have occurred to trees and other vegetation close to or downwind of high level SO2 emitters, such as the well known Sudbury smelter in Canada. The incidence of such high atmospheric concentrations in the EEC is relatively limited, but because the damage mechanisms involving high concentrations are more easily studied in laboratory experiments, they have received more research attention. 

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