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V. The Role of Stomata

V. The Role of Stomata

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Stomata1 governing of gaseous uptake can be evaluated using the gas

transfer equations of Penman and Schofield ( 195 1 ) . Simply, the expression


= DAv/(Ra

+ R , 4- Rm)

will describe ozone uptake, where Q = ozone uptake in nig cm-2 sec-l;

D = diffusion coefficient for ozone in mg ~ m mbar-l;

- ~

Av = ozone pressure

difference between source (atmosphere) and sink (reacting) surface of tissue

in millibars; R, = boundary layer resistance in sec cm-'; R , = leaf or stomatal resistance in sec cm-'; R , = residual resistance to ozone transfer beyond

Ra and R,, also in sec cm-l.

An additional resistance, R,., defined as the resistance to gas transfer

of the nonstomatal surface of the leaf, can usually be ignored since for

water vapor and CO, its value is quite high and constant. We know little

about the R,. for ozone, but Rich et al. (1970) estimated it at 19 sec cm-l

for bean plants. D,the diffusion coefficient for ozone in air is not known,

but would be an exponential function of temperature.

The rate of ozone uptake, therefore, can be increased by a variety of

means including ( a ) temperature increases that directly affect D, ( b )

increases in the amount of ozone in the atmosphere, which would increase

Av, or (c) reductions in any of the resistances, R.

The boundary layer resistance, R,, is a partial function of air movement

as well as the surface characteristics of the leaf and leaf canopy. R,, is

usually in the range of 0.1 to 1.0 sec cm-' and in still air was estimated to

be 0.6 sec cm-' for ozone by Rich et al. (1970). Hill and Littlefield

(1969) reported a severalfold increase in the rate of ozone uptake by

oat leaves with air velocities increased from near 0 to 3.0 miles per hour.

The latter conditions probably operated to reduce R,.

R,, or the stomatal resistance, is most important for our discussion since

it is the variable resistance by which gas transfer is regulated. The study by

Rich et al. (1970) strongly suggests that R , is the major resistance regulating ozone uptake by leaves since resistances for water loss and ozone

uptake are nearly the same. Furthermore, Lee (1965) constructed a curve

showing the expected ozone injury response as a function of stomatal

opening in sensitive bean tissue. This curve is exactly predicted from the

gas transfer equation. At low stomatal apertures, and hence high R,, R ,

becomes the limiting resistance and a near-linear response to gas uptake

and stomatal aperture is seen. At wider stomatal apertures and consequent

lower R , values, other resistances (i.e., the constant R, and Rm)predominate, and further increases in stomatal aperture have minimal effects. This

is why only small correlations may exist between stomatal aperture and



expected responses, such as ozone injury. It is only for low stomatal apertures that R, exerts significant control over gas transfer.

It would be difficult to evaluate R,, without knowing the site or sites of

ozone injury. If the target site was the limiting membrane of the cell, R ,

would be small and probably inconsequential. If, however, other important

sites exist, perhaps, for example, the chloroplast membranes, then R,

could be significant.



1 . Condition of Stomata

Heggestad and Middleton (1959) demonstrated the importance of R,

in governing the extent of ozone injury in susceptible tissue. The adaxial

leaf surface resistance (R,) of pinto bean leaves is near€y 50% greater than

the abaxial surface. If the adaxial surface of a susceptible leaf is coated

with petroleum jelly, then injury develops as in a control. If, however,

the abaxial surface or both surfaces are coated, ozone injury is prevented

(Evans and Ting, 1974a).

Dean (1972) determined the size and density of adaxial stomata from

two resistant and four susceptible tobacco varieties and found a reduced

stomatal density in the resistant varieties but no difference in stomate size.

2. Water Status, Humidity, and R ,

Water-stressed plants are less prone to ozone injury than those kept on

a favorable moisture regime (Heck, 1968). Seidman et al. (1965) observed that if water was withheld from petunia, bean, and tobacco plants,

fumigation with auto exhaust was not injurious. The artificial drought conditions were correlated with increased leaf resistance to gas transfer. Leone

and Brennan (1969) exposed begonia to high relative humidity and noted

enhanced injury by ozone which they correlated with decreased R,. Otto

and Daines ( 1969) positively correlated leaf permeability index (reciprocally related to R,) determined with a porometer, relative humidity, and

ozone injury, to pinto bean and tobacco leaf. The authors concluded that

humidity affected stomatal aperture.

There is yet a large body of evidence to suggest that favorable water

status predisposes plants to ozone injury beyond just stomatal effects

(Heck, 1968). For example, Turner et al. ( 1972) compared four cultivars

of tobacco, which differed markedly in sensitivity to ozone, with respect

to stomatal conductance, the reciprocal of R,. There appeared to be no

significant differences in R, among these cultivars to warrant the conclusion



that stomates accounted for the differing ozone sensitivities. However, in

a later study (Rich and Turner, 1972) comparing a sensitive tobacco strain

with a tolerant strain, stomatal resistance did appear to account for differential sensitivities. When kept in a dry atmosphere (37% relative humidity), ozonation for 120 minutes at 0.20-0.25 ppm resulted in an increased

R , for the resistant cultivar over the sensitive one (6.2 sec cm-l as compared to 3.5). Yet in a moist atmosphere (73% R H ) the difference between resistant and sensitive varieties was 4.2 and 5.6 sec cm-'. Hence

at high atmospheric moisture, these data do not necessarily support their


In another study (Ting and Dugger, 1971), water relations were

studied in the ozone-sensitive Be1 W-3 tobacco and the resistant cultivar,

Bel-B. When grown in pots, Bel-B had a significantly smaller root system

and lower leaf tissue water potentials. Concomitantly, in the light, R , was

greater for Bel-B than Be1 W-3.

In a study by Hill and Littlefield (1969), on a variety of plants including

oat, barley, wheat, tobacco, pinto bean, lima bean, chard, corn, cauliflower,

sugarbeet, potato, and tomato, ozone always decreased stomatal aperture.

Stomatal closure, estimated by fixing epidermal strips in alcohol followed

by microscopic observation, was correlated with a reduction in transpiration and net photosynthesis. Their experiments were conducted at 50%

relative humidity and 24°C.

Stomatal opening is a turgor response; positive turgor in guard cells relative to adjacent cells is necessary to bring about stomatal opening (Slatyer,

1967). Recently potassium was found to be necessary for stomatal opening, presumably by acting as an osmotic agent and/or counterion for

organic osmotic agents (Humble and Hsiao, 1970). Any substance that

interferes with water permeability, potassium transport or permeability, or

general leaf water relations, is apt to alter stomatal opening and R,. But because of the complex physical relationships between the guard cells and

adjacent cells, changes in water balance and/or membrane permeability

could result in either an increased or decreased R,.

In an early study, Dugger et al. (1962b) showed that pinto bean plants

exposed to 0.7 ppm of ozone for 30 minutes either showed no change

in leaf resistance or a slight decrease indicative of stomatal opening. In

our own study (Evans and Ting, 1974a), if pinto beans were exposed to

0.65 pprn of ozone, the adaxial leaf surface resistance did not change during a 90-minute fumigation period, but extended fumigation caused a reduced leaf resistance. The abaxial leaf resistance at 0.65 ppm of ozone

increased during the first few minutes, decreased, then increased up to 90

minutes. Exposure to 0.8 ppm caused a steady decrease in leaf resistance



of the adaxial surface. The results of Evans and Ting’s study were obtained

with a leaf resistance hygrometer (van Bavel et al., 1965) and could reflect

changes in transpiration independent of R, changes. The same results were

obtained by Dugger et al. (1962b), however, using an air flow type of

porometer described by Heath and Russel ( 1951 ) .

From previous discussion then, it is evident that for significant foliar

ozone injury to occur, stomata must be open and R , must be low, and,

in general, plants subjected to water stress or plants with inherently poor

water balance will be more ozone tolerant. It is reasonable to conclude

that ozone alters stomatal opening by directly affecting water permeability,

potassium leakage (Evans and Ting, 1973), and potassium transport

(Evans and Ting, 1974b). The degree of stomatal opening is a function

of the osmotic properties of the guard cells as governed, at least in part,

by potassium movement (Humble and Hsiao, 1970).




As observed in the above section, providing the tissue is predisposed

to injury by virtue of age or other factors, then the R , value is closely

correlated with the degree of ozone injury. Frequently, however, plants

are not injured despite the fact that we must assume ozone has entered

the leaf.

In Fig. 3, it is shown that the R, of leaves during maximum ozone

susceptibility is not significantly different from the young and old resistant

periods. Since we must assume that the same quantity of ozone entered

the leaf at day 7 as at day 10, then factors other than stomatal aperture

are responsible for the lack of susceptibility, although a slight average increase in R, after day 12 could account for some of the reduced injury.

The convincing observation made by Dugger et al. (1962b) for pinto bean

leaves was that peroxyacetyl nitrate injury occurred in leaves younger than

those injured by ozone. Hence stomatal regulation of gas transfer could

not account for the differential susceptibility between PAN and ozone.

The early study by Glater et al. (1962) showed that only expanding

tobacco leaves were susceptible to ozone injury and that recently matured

cells were injured. They concluded that the injury potential was a function

of “cellular development and maturity.” Their study further showed that

in tobacco, stomata were nonfunctional in young, nonsusceptible leaves.

They concluded that heavy deposits of suberin protected older, nonsusceptible leaves from ozone injury. Tobacco seems to differ markedly from

bean in that there are functional stomata in bean prior to the age of susceptibility (Evans and Ting, 1974a).






I . Genetic

Although there is much documentation for genetically determined oxidant resistance in plants, in few instances is there a sound physiological

or biochemical basis for the resistance. An exception, however, is the work

of Engle and Gabelman (1966), who isolated inbred onion cultivars resistant and sensitive to ozone. They observed that the sensitive inbred SW34

maintained open stomata after ozone exposure whereas stomata of the resistant inbred onion strain closed. They hypothesized that the guard cells

of the resistant plants became leaky after ozone exposure resulting in subsequent closure, after which tl.:y functioned again. Genetic crosses suggested

that resistance was controlled by a dominant genetic system, but it was

not ascertained whether resistance was a single gene trait.

2. co,

It is now generally known that high CO, results in stomatal closure and

low CO, brings about opening. Hence, Heck and Dunning (1967) exposed

pinto bean and tobacco to 500 ppm of CO, excess and observed a reduced

injury to tobacco by ozone but no change in pinto bean injury. They did

not, however, measure R , responses to CO,.

3. Chemicals

Abscisic acid (ABA), presumably because of effects on membrane

permeability, tends to close stomata (Addicott and Lyons, 1969). In one

study stomata were closed with 10 ppm of ABA to protect 14-day-old

bean leaves against ozone (Fletcher et al., 1972). Four hours after ABA

treatment, plants were exposed to 0.2-0.4 pprn of O:, for one hour. Before

ozone, the water-treated controls had stomatal apertures of 10.7 pm whereas

the ABA-treated plants had apertures of 4.2 pm. After ozone, the controls

and treated leaves were 4.9 and 2.9 pm, respectively, and the ABA-treated

plants did not show visible injury. Though no R , estimates were made,

stomatal closure was probably sufficient to account for the observed


Certain other chemicals which reduce stomatal aperture such as phosphon D, 8-hydroxyguinoline sulfate, and phenylmercuric acetate tend to

protect against smog injury (Seidman et al., 1965). The feasibility of using

such compounds to prevent oxidant injury has not as yet been pursued

in depth, but may be a promising approach. Unfortunately, plant productivity also declines with these chemicals due to lack of CO,.





In general, the oxidants ozone and peroxyacetyl nitrate cause a variety

of injury symptoms in plant tissues ranging from excessive water loss, impairment of photosynthetic activity, an imbalance of metabolites, a reduction in cell wall biosynthesis, and finally to cellular collapse and visible

necrosis. Visible injury always results in a reduction in growth and, in the

case of valuable crop plants, a reduction in yield and quality. Most of the

symptoms described above are probably of a secondary nature and do not

reflect the primary target sites.

It is our hypothesis that oxidants initially alter the selectivity of limiting

cellular membranes such that solutes and salts leak from or into organelles

and cells. The resulting imbalance of ionic potential anJ water balance

is manifested first by leakage of potassium from the cells followed osmotically by water. This initial loss of membrane differential permeability produces other biochemical effects which ultimately cause necrosis or cellular

collapse and death of the tissue. Just why these oxidants should alter membrane selectivity is not known for certain but could be related to the oxidation of the sulfhydryls or unsaturated fatty acids of the membranes.

Given our present economic and technological status, it is rather unlikely

that increasing air pollution will be little more than slowed in the near

future. In fact, there is no real attempt to eliminate pollution, but simply

to meet air quality standards of a tolerable level and ones that are acceptable with respect to human health alone. Although rather pessimistic, a

reasonable agricultural goal is to develop pollution-resistant crops that can

grow and maintain high yields under a variety of pollution conditions. We

emphasize that the only way to achieve this goal is by the cooperation

of physiologists and geneticists. Further work must be done to allow US

more fully to understand the biochemical and physiological basis of air

pollution injury. The hypothesis we present concerning oxidant alterations

of membrane permeability is merely a beginning. Future physiological and

biochemical information can and should be used by the geneticist in

thoughtful breeding programs.


Both authors wish to acknowledge a major indebtedness to W. M. Dugger, Jr.,

who began much of the work described here and who still is a major contributor

to the thrust of this research. Over the years in our laboratories a number of people

have contributed significantly to our understanding of the mechanism of oxidant

injury to plants; among them are: C. Coulsen, P. Chimiklis, L. E. Evans, P. Frederick, F. Fong, R. Gross, J. Koukel, S. Lackey, S. K. Mukerji, J . Perchorowicz,



J. Vereen, and R. Sutton. We also thank our many colleagues including J. B. Mudd,

L. Ordin, R. Palmer, 0. C. Taylor, and W. W. Thomson for many helpful discussions.

Much of our own research was supported by Federal Grants from the following

agencies: NAPCA, USPHS, EPA, and USDA.

We especially thank Ms. Paula Frederick for her editorial efforts during the preparation of this manuscript.


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V. The Role of Stomata

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