plants under stress
TRANSCRIPT
PLANTS UNDER STRESS
desert
Arid zone
Salty soilAntarctic region
What is Stress?
• A significant deviation from the conditions optimal for life, and eliciting changes and responses at all functional levels of the organism.
• Two ways
Temporary stress
Permanent stress
What Happens During Stress?
How to Recognize Stress
Effects of Stress 1. Stressor-specific effect
involve a well- defined target within the plant.
Ex. Intense radiation causes direct damage to the thylakoidmembrane
2. Non- specific effect Stress responses within the plant is carried out
by phytohormones.
How to Recognize Stress
• Non- specific effects of stress
a. Alterations in membrane properties (membrane potential, transport of substances)
b. Increased respiration
c. Inhibition of photosynthesis
d. Growth disturbances
e. Lower fertility
f. Premature senescence
g. Decrease of availability of energy
How to Recognize Stress
• Intracellular decrease in availability of energy. (Due to metabolic impairment)
• Less ATP is formed.
• It can be calculated as an Adenylate Energy Charge(AEC).
AEC = (ATP)+ 0.5(ADP)
(ATP)+(ADP)+(AMP)
• AEC < 0.6 indicates deterioration in the vitality of a plant, and a plant under stress.
Survival of Stress
• Survival = Stress evasion, Resistance, Recovery
Natural Environmental Constraints
• Environmental stress factors
1. Abiotic factors – mainly include climatic factors.
2. Biotic factors – Due to activity of animals, microorganisms or human beings.
Multiple Stresses
• In nature frequently multiple stresses are involved.
Ex. Stress arise due to combination of strong radiation, overheating, drought in open habitat.
Radiation Stress
• Two ways of radiation stress
1.Excessive quantities of photosyntheticallyactive radiation.
2.increased absorption of UV radiation.
Light Stress
• Strong light presents the leaf with more photochemical energy than can be utilized for photosynthesis.
• Overloading of the photosynthetic process.
• Extremely high irradiance destroys photosynthetic pigments and thylokoidstructures is called “photodamage”
• Shade plants may be damaged breif exposure of strong light.
Light Stress
Conostomum tetragonium exposed to the high light intensity
Photoinhibition
• Inhibition of photosynthesis caused by excessive radiation.
• Strong light attack photosystem II
• Brake down of Protein sub units
• Photosynthetic electron transport is interrupted.
• Reduce efficiency of photosystem II
Photoinhibition
As an protective measure,
• Excessive radiation energy is diverted to fluorescence and heat.
• Surplus reductive capacity in chloroplast is used by “Xanthophyll Cycle”
Xanthophyll Cycle
Thylakoid membraneLumen Stroma
A moss quenches high light energy with the pigment zeaxanthin.
a) Pellia endiviifolia did not experienced a rise in de-epoxidized Xanthophyll.
Liverworts
b) Flullania dilatata was a rise in the concentration of de-epoxidized xanthophylls that can protect cell from chlorophyll damage
a)
b)
Adaptation to Stress from Strong Light
• Positioning leaves at an angle to the incoming light- Receive less radiation.
• Rolling up the shoots (mosses, pteridophytes) • Dense coverings of trichomes on the upper
surface of the leaf. • Thickened walls in the epidermis and hypodermal
tissue-act as diffusive filters (conifer needles & cacti)
• Presence of Anthocyanin- act as darkening filters & shields the mesophyll.
Ultraviolet Radiation
• Two types of UV radiation
UV-A (315-400nm)
UV-B (280-315nm)
• UV-A is mainly photooxidative.
• UV-B is in addition to photooxidative action causes photolesions in biomembranes.
UV Damage
• Breaking down the disulfide bridges in protein molecules.
• Dimerizing thymine groups of DNA- results in defective transcription.
• Xanthophyll cycle is disrupted by inhibiting the violaxanthine-deepoxidase
UV Damage
Can be identified by
• Changes in enzyme activity (increased peroxidase activity, inhibition of cytochromeoxidase).
• Poor energy status of the cell.
• Lower photosynthetic yield.
• Disturbed growth (reduced extension growth & pollen tube elongation).
PLANT STRESS DUE TO EXTREME TEMPETURES
24
KINETIC ENERGY OF MOLECULES= HEAT
KINETIC ENERGY OF MOLECULES
HIGH ENERGY
LOW ENERGY
HEAT
COLD
25
Temperature balance on earth by,Solar radiationair current
Heat and Cold effect• Metabolic activity• Growth• Viability • Distribution,
of a plant.
26
Critical temperature Thresholds
• Activity limit
(5-25 0C)
• Lethal limit
– Cold
– Heat
27
28
Heat
Highest temperature on earth- 80oC
Lethal limit- 40-70oC
High temperatures arise by,
• Higher solar radiation
• Volcanic phenomena
• Hot pools
• Fires
29
Functional disturbance of heat
• Damage physiochemical state of bio membranes and the conformations of protein molecules.
– Disturbance in photosynthesis
– Disturbance in transport
– Disturbance in mitochondrial respiration
30
Heat Tolerance
• Evasion of strong sunlight– Thick cutine layer
• Heat insulating bark– Thick fibrous bark– Rough suberized bark– Silica in cell walls– Peripheral cambium layer
• Dense leaf sheaths covering the basal buds• Withdrawal to underground organs• Transpirational cooling
31
Most effective form of heat protection is provide by,
Heat shock proteins
32
Type of heat resistance
Three types
• Heat sensitive species
• Relatively heat resistant eukaryotes
• Heat tolerance prokaryotes
33
Cold
lowest temperature on earth= -90oC
Lethal limit= +5 - -90oC
low temperatures arise by,
• Low solar radiations
34
Functional disturbance of cold
Above the freezing pointBy Decrease the speed of chemical reactions
• Uptake of water and nutrients restricted
• Less metabolic energy
• Less biosynthesis
• assimilation reduced
• Growth stops
35
The first main detectable result of low temperature is,
cessation of cytoplasmic streaming
36
Mostly effect on chilling sensitive plants. It happens in stepwise
37
Primary effect:-LIQUID CRYSTALINE BIO MEMBRANES → SOLID GELL
Initial reversible processes:-DAMAGE TO THE FUNCTIONALITY OF ORGANS
CLOROPLAST- INHIBIT PHOTOSINTHESISMITOCHONDRIA- INCREASE RESPIRATION
Final irreversible processes:-INSUFFICIENT CARBOHUDRATES
IMPAIRED ION BALANCEIMBALANCE IN METABOLISM
ACCUMILATION OF TOXIC SUBSTANCESINJURY AND DEATH OF CELLS
Type of chilling sensitive plants
• Partially sensitive plants
• Totally sensitive plants
38
Below the freezing pointFROST OCCUR PERIODICALLY AND EPISODICALLY ON EARTH
by the ice formation
• Cytoplasm destroy by ice crystals
• Block the vascular bundles
• Ice nucleation active bacteria attack
39
By ice formation less water in the plant = Desiccation condition arise
40
It results,
• Unfrozen solution reach abnormally high concentration
• Toxic effect
• Enzymes get inactive
• Bio membranes are overtaxed both osmotically and by the volume reduction
41
Freezing of cells
• intercellular • Extracellular
42
Low temperature tolerance• No thermal insulation (no heat losses)
– Dense growth surrounding the regenerative buds
– Giant rosette
• Abscission of sensitive organs
• Depression of freezing point
• Super cooling
• Trans located ice formation (extra tissue freezing)
43
Categories of cold resistance
• Chilling sensitive plants
• Freezing sensitive plants
• Freezing tolerance plants
44
EVOLUTION OF VASCULAR PLANTS FOR FROSTHappen in a stepwise process
45
First step:COLD ADAPTATION OF ENZYMES AND MEMBRANES
Second step:IMPROVING THE SUPERCOOLING CAPACITY
Survival capacity
• Younger plants are more sensitive
• Reproductive organs are more sensitive
• Underground organs are also quite sensitive
• Above ground shoot is the least sensitive part
46
Winter desiccation
Winter conditions may result in damage due to desiccation.
This happen by,
• Frozen soil
• Snow and ice
47
Effects of winter desiccation
• Plants can not take up enough water and nutrient
• Loss water by stomatal transpiration
• Xylem transpiration make cavities of the water columns in the conducting vessels
• Block the passage of water through the xylem
• Chronic damages in plant tissues
48
Harmful effect of long periods beneath ice or snow
• Low CO2 and O2 permeability of ice sheets
• Stop the gas exchange of plant
• Respiratory CO2 increase and O2 decrease with in the plant
• Hypoxia
• Toxic substances accumulate
• Pathogenic effect
49
Oxygen Deficiency in the Soil.
Drought
Salt Stress
Oxygen Deficiency in the Soil.
Lack of sufficient oxygen in the soil.
Extensive areas of land are temporarily inundate by
flood waters of large rivers, small rivers or streams
repeatedly overflow their banks.
the plants cover of valley soils is often buried of long
period of times.
Soils are compacted and become impermeable as a result
of construction activities.
The soil atmosphere is low in Oxygen in any
case,
Anaerobic microorganisms take over .
Creating a strongly reducing milieu which Fe2+ ,Mn2+
, H2S, Sulphides ,Lactic acid ,Butyric acid are present in
toxic concentration.
Nitrogen turnover in the soil.
Functional Disturbances and Patterns of
Injury
roots are capable of respiring anaerobically,
continuous for some hours irregularities in metabolism
occur.
partial pressure of Oxygen drops to 1-5 kPa (Hypoxia)
Alternative respiratory pathway is activate.
The energy status of the adenylate system drops
substantially.
Root growth stops.
Root tips entering the low Oxygen zone die off
Adventitious root developed.
Older part of the root systems often develop corky
intumescences and swollen lenticels.
Total and near total Oxygen deficiency (anoxia)
Respiration switches to anaerobic dissimilation
In the absence of terminal oxidation
Acetaldehyde and ethanol accumulate.
Abscisic acid, ethylene and ethylene precursors are
formed in larger amount.
Evoking in the leaves partial stomatal closure.
Epinasty and often abscission.
Cellular membrane systems brake down.
Mitochondia and microbodies disintegrate and their enzymes
are partially inhibited.
Fig. 6.51
Surviving Oxygen Deficiency
Many plants can germinate, roots and grow in oxygen deficient
soil because they have developed certain adaptations to meet
conditions in an toxic environment.
Functional adaptation Morphological
adaptation
Functional adaptation
increase in alcohol dehydrogenase (ADH) during
anaerobiosis.
Protein metabolism is adjusted within a few hours
after gene activation
Morphological adaptation
A hypoxic milieu consist in the development in ventilating
tissue (aerenchyma) with a continuous systems of
intercellular spaces.
The volume of intercellular system in the root parenchyma,
swamp plants – 20%-60%
well-aerated plant – <10%
Well aerated roots may even loss oxygen to the surrounding
soil, It can detoxify harmful reducing substances :
Fe2+ Fe111- oxide.
Aeration is also furthered by temperature gradients.
Plants growing on very dense and poorly aerated soils develop
a system of laterally spreading roots near the surface.
In the flooded regions submerged parts of trunks and
branches put out dense bundles of water roots.
poplar, willow, alder, ash
In mangrove plants,
In the form of lenticels-covered respiratory roots
(pneumatophores) with a large amount of aerenchyma.
Knee roots that produced above the surface of the soil and
standing water.
Drought
A period without appreciable precipitation, during with the
water content of the soil is reduced to such an extent that
plants suffer from lack of water.
Low precipitation and high evaporation.
Strong evaporation caused by dryness of the air and
high levels of radiation.
The dry region of the earth
Functional disturbance and patterns of Injury
Decrease in turgor and a slowing down of growth process
Decrease in cell volume
Most strongly inhibited enzyme is nitrate reductase.
plants that have been treated with nitrogen containing
fertilizer in drought.
Nitrogen fixation is more sensitive to drought.
Increase in concentration of the cell sap.
Progressive dehydration of the protoplasm
Protein metabolism and synthesis of amino acids are
impaired.
Supresses cell division
Slow down mitosis- S phase being affected most.
During pollen development, the meioses exhibit
chromosome anomalies- specially metaphase and anaphase.
Drought lower pollen fertility.
During drought,
Initiate stomatal closer
Under the influence of hormone synthesized in the
leaves and roots in response to drought
Changes occur in the allocation of assimilates
The ratio of shoot to roots growth is altered
Characteristic morphogenetic features develop
Reproductive processes become predominant
Senescence is accelerated
Older leaves dry out and shed
In wilt,The reduction of cell volume
Increasing concentration of the intercellular solutes-ions
In the final phase preceding cellular disruption
The central vacuole splits up into small fragmentary
vacuoles
The thylakoids in the chloroplasts and the mitochondrial
cristae first of all swell and are later break down
The nuclear membrane becomes distended and the
polyribosome disintegrate
Drought stress in tobacco
Fig. 6.62
Survival of Drought
Drought resistance
the capacity of a plant to withstand period of dryness, and is
a complex characteristics.
xerophytes
Desiccation Avoidance
desiccation is delayed by all those mechanisms
that enable the plant to maintain a favorable tissue water
content as long as possible despite dryness of air and
soil.
uptake of water from the soil
reduced loss of water
Water uptake
extensive root system with a large active surface area is
improved further by rapid growth into deeper soil layer
the seedling of woody plants in dry regions may have
tap roots ten times as long as the shoot
grasses in such places develop a dense root system and
send their threadlike roots to depths of some meters.
Fig 6.64
Reduction of transpiration
Modulative adptation
timely closure stomata
when leaves growing under conditions of water
deficiency develop smaller but more densely distributed
stomata.
Fig 6.65
The leaves have more densely cutinized epidermal walls
Covered with thicker layer of wax.
Stomata are present only on the under side of the leaves
smaller
often hidden beneath dense hair or in depression
Boundary layer resistance is increased and the air outside the
stomata become moisture
Rolling the leaves
Salt stress
Salt stress may have be a first chemical stress
factor encountered during the evolution of life on earth.
Saline habitats
the presents of an abnormally high content of
readily soluble salt
Aquatic saline habitat: Oceans, salt lakes, saline ponds
In land: saline soil
Effect of high salt concentration on plants
The burden of high salt concentrations for plant is due to
osmotic retention of water and to specific ionic effect on
the protoplasm.
An excess of Na+ and Cl- in the protoplasm lead to
disturbance in the ionic balance
Ion specific effects on enzyme protein and
membrane.
Too little energy is produced by photophosphorylation
and phosphorylation in respiratory chain
Nitrogen elimination is impaired
Protein metabolism is disturbed
Accumulation of diamines such as putrescine
cadaverine,polyamines
Functional disturbance
Photosynthesis is impaired
Stomata closure
Effect of salt in chloroplast in particular on electron
transport and secondary process
Respiration increased or decreased – root
Enzyme system of glycolysis and the tricarboxylic acid
cycle are more sensitive than alternative metabolic
pathways.
When the NaCl content of the soil is high the uptake of
mineral nutrients NO3- , K+ , Ca2+ is reduced.
Extreme salt stress
Inhibition of root growth
Bud opening is delayed
Shoot are stunted
Leaves are small
Cell die and necrosis appear in roots, buds, leaf margins and
shoot tips
The leaves become yellow and dry before the growing
season has ended and whole portion of the shoot dry out.
Lower level of cytokinin
Increased abscisic acid senescence
Survival of Saline habitats
plant growing in saline habitat cannot evade the
effects of salt and must therefore develop at least some
degree of resistance to it.
Salt resistance is ability of a plant either to avoid,
salt regulation
excessive amount of salt from reaching the
protoplasm
to tolerate the toxic and osmotic effect associated
with the increased ion concentration.
Regulation of the salt content
1. Salt exclusion: In some mangrove- transport barriers of the
roots prevent the salinity of the water in the conducting
system from becoming too high.
Prosopis farcta
crop plants
halophorbic species
2. Salt elimination : A plant can rid itself of excess salt ,
releasing volatile methyl halides –
exclusion by glands
excretion of salt at the shoot
shedding parts heavily loaded with salt
marine phytoplankton
macro algae
fungi
3. Salt redistribution:
Na+ and Cl- can be readily translocated in the
phloem , so that the high concentration arising in actively
transpiring leaves can be diluted by throughout the plant.
4. Salt tolerance : the protoplasmic compartment of
resistance to salt stress.
Anthropogenic stressMan made pollutants and their impact on the phytosphere.
Due to human activities plants exposed to greater amounts of harmful substances.
Human activities…
• Results of industrial processes.
• Traffic.
• Chemicals used in agriculture and household, fertilizers, pesticides.
• Excessive consumption of fossil fuels-emmission of green house gases.
• Catastrophic accidents-nuclear reactor activities, oil spills.
• Pollutant
A contaminant of air, water or soil that has an adverse effect on an organism.
1.Naturally occurring pollutants
2.Anthropogenic pollutants
Instead of one pollutant activity combined activity of pollutants.
Ex: Photo oxidant complex + SO2 (g),+ heavy metals
Naturally occurring harmful substances in higher concentrations.
• SO2 (g),NO2 (g),H2S (g),O3 (g)
• Dust.
• Heavy metals.
Ultimate result is environmental stress.
Ecosystems
Countries
Continents
Entire globe
• High input of pollutants within a short period of time = acute damages
• Exposure to low concentrated pollutants for a longer period of time = Chronic damage
Pollution Injury
The extent which vital(physiological & biochemical) functions are affected.
Visible damage depend on many factors of the plant.
1. Plant species.2. Growth form.3. Age of the plant.4. Phase of activity.5. General vigour(physical strength & good health.6. Climatic and edaptic condition.7. Chemical nature.8. Concentration of the pollutant.9. Time and duration of the action of the pollutant.
Air born pollutants
• SO2 (g),NOx (g), PAN (peroxyacetylnitrate),Hydrogen helides, NH3(g), hydrocarbons, tar fumes, soot, dust.
Symptoms of damage
• Non specific.
• Many symptoms interact with other plant stress factors.
• At noon stomata are fully open atmospheric pollutant concentration is high in noon damage is higher.
• At night plants recover from the injurious immisions.
Early recognition of pollution damage1. Accumulation of toxic compounds/substances in the
plant tissues.2. Reduction of buffering capacity of tissues.3. Erosion of epicuticular wax .4. Decreation /incretion of certain enzyme activities.5. Qualitative and quantitative shifts among
metabolites.6. Appearance of stress hormones– Ex: ethylene7. Respiration incretion/decreation8. Photosynthetic disturbance.9. Alteration of stomatal opening and closure.10. Diminished allocation of photosynthetes to the root
system.
When the pollutant in immediate vicinity..
1. Occurrence of chlorosis.
2. Leaf discoloration.
3. Tissue necrosis.
4. Death of entire plant.
•Reduce productivity and defective fertility.
•Less growth in cambial tissues.
•Foliage become sparser.
•Water transpiration interfered.
SO2 (g) –cause most of the damage
Natural sources-volcanic emissions, S containing ores, biological decay and forest fires.
Man-made sources-fossil fuel combustion, smelting, manufacture of sulfuric acid.
SO2 (g) is there in the environment since the plants beginning.-Plants have been adapted to tolerate SO2 (g) for some extent.
Entry into plants.
1. Enter the leaf through opened stomata.
2. By over-coming the cuticular resistance.(if the stomata are closed)
Damage by SO2 (g)
SO2 (g)
low external concentration
Trigger a loss of turgor in epidermal cells
Stomata open
Transpiration high
• High external concentration
• Stomata closure
• Low transpiration
• SO2 (g) diffuse similar as CO2 (g) .
Atmospheric SO2 (g)
Dissolved in guard cell wall water SO2 (g) +H2O(l)
HSO3-(aq) + SO3
2-(aq)
Chloroplast: Cytosol: Vacuole96 : 3 : 1
Sulphur compounds (SO2(g),H2S (g) )detoxification
01.) SO32-
(aq) SO42-
(aq)
SO32-
(aq) remaining will effected by the photosynthetic sulphur metabolism
Covert to sulphur containing amino acids.(cysteine, methionone)
Call wall peroxidases.
Harmful effects of SO2 (g)
1. SO32-
(aq) Level in chloroplast rise.
2. SO2(g) ,occupies binding sites in RUBP carboxylases.
secondary process of photosynthesis inhibits.
3.The tertiary structure of the enzymes are disturbed.
4. SO32-
(aq) SO42-
(aq)
Super oxide radicals generate, if not excluded rapidly chlorophyll will be destroyed.
photooxidation
Mechanisms of resistance of SO2 (g)
stress* can be passive or active processesPassiveNon specific, not usually related
to a particular pollutant.1. Regular development of new
leaves with short functional life span.
Ex: deciduous
woody plants
• Thallophytes also have structural, chemical characteristics reduce the entry of SO2
ActiveStressor specific processes.1. High buffering capacity-from
increased uptake of alkali & alkali earth cations.
2. Binding to 2ry products of metabolism.
3. Metabolic use of Sulphur and detoxifying oxidative reactions.
4. C4 syndrome.
Ever green trees with needles
Ever green tree s with needles Deciduous woody plants
C4 syndrome
C4 grass
1.Miscanthus sinensis
2.Andropogon virginicus
Moderate resistant C3
1.Polygonaceae
2.Metrosideros collina in Hawaii
Some plants have the ability to grow in the vicinity of volcanic vents
Species-specific sensitivity to immissions.
• Different species
• Individual varieties and ecotypes
• Different life stages
SO2 (g) Resistant plant species introduce to
polluted areas.
Highly sensitive plants to SO2 (g) Indicator organisms to indicate SO2 (g)
pollution.
Atmospheric oxidants and secondary photooxidants.• O3(g) ,NOX(g) (NO(g) ,NO2(g)),peroxy radicals.
• NO2(g) NO(g) + O.(g)
• O. (g) + O2 O3(g)
• NO(g) + O3(g) NO2 (g) + O2(g)
Peroxy radicals +hydro carbon compounds
UV 300-400 nm
Peroxyacetyl nitrtes.Peroxybutyl nitrates.Peroxybenzyl nitrates.
Uptake by the plant
• Through opened stomata.
• NO2(g) diffuse through cuticle, much faster than SO2(g) .
• O3 (g) dissociate to O2(g) in the outer wall of the epidermis.
• NO(g) ,NO2 (g) NO3-(aq) ,NO2
-(aq) with water
taken up actively by living cells
Events within the cell.
• NO3-(aq) amino acids.
* SO2 (g) inhibit the action
of Nitrite reductase.
• Additional source of nitrates-advantageous.
• Acidification of cells/leaves-disadvantageous.
Nitrite reductase enzyme
Toxicity of nitrates
O3(g)
• O3(g) O2(g) + O.
• Peroxides,
-effect on plasma membrane.
-other bio membranes.
Transfer process impaired.
Necrosis,growthreduction,lessyields
Heavy metal contamination of soil, water
Create long term problems
metals = Zn,Pb,Ni,Co,Cr,Cu
Metalloids = Mn,Cd,Se,AS
Accumulation in organisms, circulate in food chains.
Common heavy metal sources1. Industrial zones.
2. Heavy vehicle traffic.
3. Sewage sludge.
4. Emissions of dust from metal processing industries.
5. Waste water-Cd,Zn,Fe,Pb,Cu,Cr,Hg
Uptake and toxic effects
• Uptake is mainly by roots.
-can’t stop the enter of heavy metal completely.
-need to plants as micro elements.
Toxicity due to..
1. Interference with electron transport in respiration an photosynthesis.
2. Inactivation of vital enzymes.
Possible mechanisms of resistance • Natural heavy metal exposures, plants growing on,
a. Metal ores.
b. Serpentine soils.
c. Strongly acidic soils.
Adaptations.
1. Immobilization in cell wall.
2. Obstruct permeation across the cell membrane.
3. Formation of chelates.
4. Compartmentalization in vacuoles.
5. Active export.
6. Characteristic patterns of iso-enzymes-element specific resistance.
7. Genetic plasticity, with several resistance genes-resistant to several heavy metals.
*these plant can be used to re-vegetation of strongly heavy metal contaminated area.
Ex:
Agrostis tenuis Festuca ovina Silene vulgaris
Bioindicators of pollution impact
• Bioindicators are organisms or communities of organisms that are sensitive to pollution stress and respond by alteration in their vital processes or by accumulation of the pollutant.
Bioindicators
•Indicator organisms- respond to their surroundings, depending on their specific requirements
•Test organisms- high degree of sensitivity to certain pollutants.
•Monitor organisms- specific responses to pollutants can be con be used for qualitative & quantitative detection of stress situations.
Indicator organisms
Accumulation of heavy metals influenced by ..1. Meteorological factors
2. Edaphic factors -Influenced by the soil rather than by the climate.
3. Habitat related factors- growth form and rooting pattern.
Heavy metal indicators= metallophytes.
Ex: Eichhornia crassipes
Reasons for forest decline
1. Ageing of the stand.
2. Episodic damage by pests.
3. Extremes of climate.
4. Inappropriate management.
5. Interruption of mineral recycling.
6. Exhaustion of soil nutrients.
7. Toxicity caused by identifiable local emitters.
forest decline
• Depend on the,
1. Tree species.
2. Growth form.
3. The site.
4. Type of the soil.
5. Geological origin.
6. Superimposition of various stress types.
Symptoms of forest decline
1. Anomalous growth.
2. Discoloration of needles and leaves.
3. Necrosis of isolated areas of needles, leaves, branches.
4. Shedding of leaves.(thinning of crown, bareness of the hanging branches).
5. Dieback of leader and branch tips.
6. Increasing the shallowness of the root system.
Causes of forest decline.
• Acidic effect of precipitations.
Direct acid damage1. necrosis of margin of leaf
2. destruction of the cuticle and cuticular waxes.
3. acidification of the apoplast– affect the distribution of phytohormornes.
4. fine root chromosome anormalities during cell division.
5. cells damage dissolution of cell walls tissue disruption.
Effect of atmospheric pollutants on the ecosystems and at the global level.
1. Acid precipitations
Green house effect
• provides temperature necessary to support the life on earth.
• Green house gases
1. CO2(g)
2. H2O(g)
3. CH4(g)
4. O3(g)
5. N2O(g)
Green house effect
References:1. http://www.hindawi.com/journals/jb/2012/872875/
(15.10.2012)
2. http://lqma.ifas.ufl.edu/Publication/BB-02.pdf (15.10.2012)
3. http://www.hokkaido-ies.go.jp/seisakuka/acid_rain/Acidrain-e.html (15.10.2012)
4. Larcher W., Physiological plant ecology, 3rd edition,Springerpublications,Berlin. pp 321-449.