Plants leaf tissue injuries

Acute S02 injury on broad-leaved plants may develop marginal or intracostal necrotic areas. Tissue along either side of the major veins is usually not affected, making the veins stand out clearly on the ivory-colored, necrotic background. Sulfur dioxide will react with water after entering leaf tissue to form sulfite ions which are subsequently slowly oxidized to sulfate. Both sulfite and sulfate ions are toxic to plant cells, but the former is reported to be as much as 30 times more toxic than the latter (16). 

Susceptibility of leaf tissue to N02 injury is increased under conditions of low light or in total darkness. Comparable injury may be produced by one-half that amount of N02 in the atmosphere on a dark, cloudy day compared with a bright, sunny day. Apparently, a light-dependent enzymatic reaction will reduce nitrites produced from foliar-absorbed N02 to the ammonia form which is readily used as a plant nutrient. Under low light this reaction is suppressed, and toxic levels of nitrites are allowed to accumulate. 

One of the earliest indications of ozone injury on several plant species is an upper surface discoloration with a waxy appearance. This symptom often disappears completely a few hours after exposure is terminated. High dosages of ozone cause permanent necrotic lesions on susceptible leaf tissue. Permeability of cell membranes is apparently disrupted, and cell contents are allowed to leak into the intercellular spaces producing a water-soaked appearance. Upon drying, the tissue will totally collapse and turn white or various shades of brown. Lesions which extend through the entire thickness of the leaf are commonly referred to as bifacial... 

Bressan, R.A., LeCureux, L., Wilson, L.G., 1979. Filner. Ph., Emission of ethylene and ethane by leaf tissue exposed to injurious concentrations of sulfur dioxide or bisulfite ion. Plant Physiol. 63, 924-930. 

Leaves of pin oak showed a different sequence of steps in leaf injury from that seen in other plant species. Initially, injury began with collapse of adaxial epidermal cells. Initial lesions consisted of approximately one to six collapsed epidermal cells which resulted in a slight depression on the leaf surface. At this stage, all cells in the mesophyll layers, and the abaxial epidermis were unaffected. After several more simulated acid rainfalls larger lesions, with increased surface area and depth, developed from smaller lesions. These lesions encompassed five to fifteen collapsed epidermal cells. Penetration of acidic solutions into the mesophyll tissues resulted in collapse of epidermal and underlying palisade parenchyma cells. 

Sulfur Dioxide. S02 injury on plants has received much attention, particularly during the past half century, and the toxic effects are well known. Symptoms of acute injury to specific crops have been described by investigators in several countries (2, 3, 4, 6, 7, 8, 15). Acute necrosis results from rapid absorption of S02. Once S02 enters the mesophyll tissue, it reacts with water to produce the sulfite ion which has strong phytotoxic properties. When lethal concentrations accumulate in the most susceptible areas of the leaf, a dark green, water-soaked discoloration develops. The affected area soon becomes flaccid, and upon drying becomes white to ivory on most plants. In some instances the dead tissue may turn red, brown, or almost black. 

On iris, gladiolus, tulip, and similar plants susceptible to fluoride injury, a narrow, dark-colored band often separates the dead and living tissue, and a series of these bands will develop as new tissue is killed by continued accumulations of fluorides. Similar bands may develop on leaves of susceptible woody species, but the necrotic tissues may also break away in a few days, leaving an irregular leaf margin. The leaf seldom separates from the tree because of the injury unless extremely high atmospheric concentrations of HF have occurred. 

Acute injury on parallel-veined leaves of monocotyledonous plants typically develops at the tip of the leaf blade. Repeated exposures to lethal dosages of fluoride will extend the necrotic lesion toward the base of the blade. Sometimes the lesions extend farther down the leaf margin than nearer the midvein, and often the lesion on one margin will extend farther down than on the opposite side. Living and dead tissue is usually separated by an abrupt line of dark-colored tissue. Successive fumigations often produce a series of these dark-colored bands. 

The experimental results demonstrate that initial injury to foliage by simulated acid rain preferentially affects the leaf indumentum near trichomes and vascular tissues. Characteristics of the adaxial leaf surface are probably important after one or two rainfalls. However, after many rainfalls, in which epidermal cells are injured, other characteristics of the leaf may become important. In general, foliage of plant species that exhibits extensive hyperplastic and hypertrophic responses has less injury than foliage of species that have these two responses. In this manner, the hyperplastic and hypertrophic responses of foliage may alleviate extensive foliar injury. 

Hydrogen sulfide at levels well above ambient concentrations destroys immature plant tissue. This t5 e of plant injury is readily distinguished from that due to other ph5dotoxins. More-sensitive species are killed by continuous exposure to around 3000 ppb H2S, whereas other species exhibit reduced growth, leaf lesions, and defoliation. 

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