Phase Transition in Membrane Lipids Associated with Chilling Damage in higher plants

Chilling damage is a physiological defect in higher flora brought about by contact to low temperatures just above freezing point. Some crops of commercial importance are affected by temperatures below 150 Celsius. This is known as chilling injury. Crops affected include sweet potatoes, sugar cane, sorghum, potatoes and maize among others. Indications of such injury consists of partial growth of photosynthetic material, pitting of the outer layer of plant, staining and uncharacteristic ripening of the fruits as well as lack of plant protection against most fungal diseases.

According to Sharom, Willemot  Thompson (1994), broad- angle x-ray gave proof of lipid stage severance in covering of microsomes of chill-damaged tomato fruit. Fully developed fruits were kept at temperatures of five degrees Celsius and developed no symptoms of chilly injury. However, after the same fruits were placed at temperatures of twenty-five degrees Celsius, signs of typical chilly damage occurred. These signs were fully recognized after four days of exposure to room temperature. Phase change and side phase division are thought to be actions leading to chilling damage signs. Side phase division of the two layers of lipid caused leaking of the membranes. Proof for chilling damage is indicated by oozing of electrolytes, lipid phase switch at decisive degrees of hotness, electron turn reverberation and switch in lipid constitution. It is also shown by fluorescence depolarization and also by chill fracture electron microscopy which help to see tangential phase separation of lipids found in the membrane. Not long ago, decreased chilling damage has been observed in genetically modified plants with lowered fatty acid concentration.

During chilling injury, hydrophobic bonds in proteins become weak and hydrogen bonds become more stable. Thus enzymes fail to function due to interruption of regions not attracted to water, or due inactivation and establishment of new hydrogen bonds and structure stabilization as a result of strengthened hydrogen bonds. The alteration in steric orientation of proteins during freezing affects physiological processes of plants. During chilling injury, biosynthesis of adenine tri-phosphate is reduced and later, ATP depletion occurs and cells die. Generally, due to high temperatures, the plant metabolic rates are lowered and there is retarded plant growth.  

Generation of Reactive Oxygen Species (ROS) in Response to Stress in Higher Plants
Generation of oxygen reactive species in higher plants has been attributed to stresses from living things and non-living things. A two phase oxidative explosion occurs in plant cells when a microbe which cannot infect is sensed. The organelle level and means of reactive oxygen species development is not fully understood.
Various strategies are associated with development of pathogen induced reactive oxygen species. These include different oxidizing enzymes and those which breakdown hydrogen peroxide. An origin of reactive oxygen species has been observed from tobacco epidermal cell. The correlation involving an infectious microbe reaction and respiration is supported by the fact that salicylic acid hampers adenine tri-phosphate synthesis and consumption of respiratory oxygen in tobacco cells not associated with photosynthesis.

Mitochondria act as origin of reactive oxygen species. It is suspected that mitochondria takes part in oxidative explosion in presence of avirulent pathogen. In breakdown of carbohydrates, the resulting oxygen molecule is univalently reduced in the location where respiratory oxygen species is generated. The superoxide results at stages I and III of carbohydrate metabolism process. This superoxide forms hydrogen peroxide which causes programmed cell death. To cause this, higher amounts of hydrogen peroxide are required because it is highly broken down by plant antioxidant systems. The process of cell death can be stopped by hindering protein synthesis since it requires functional cellular metabolism. Like in soybean cells, hydrogen peroxide stimulates Cys proteases which cause programmed cell death. Cys proteases lead to formation of Cytochrome C from power houses of the plants.

As noted earlier, mitochondria play a vital role in generation of reactive oxygen species. Placing Arabidopsis cells in continuous oxidative strain enhances electron transport during respiration. It causes high oxygen intake thus the formation of reactive oxygen species which intensify oxidative strain. Hydrogen peroxide induces leakage of the mitochondria and liberation of cytochrome c from inner membrane leading to lack of adenine tri-phosphate and consequential cell death. Jamming of mitochondrial permeability transition pore by use of cyclosporin A inhibits cell death.

Reactive oxygen species in plants is as a result of byproducts of several metabolic processes in various organelles of the cell. In normal conditions, these byproducts are neutralized by antioxidants found in those organelles. Plants have a well developed defense mechanism against generation of reactive oxygen species. The mechanisms control accumulation of hydrogen peroxide, formation of iron inions and superoxide.
The mechanisms include non-protein antioxidants and antioxidants which are proteins in nature. Non-protein antioxidants comprise of glutathione and vitamin C. It also includes alkaloids, flavonoids, tocopherol and carotenoids. Vitamin C and glutathione act as buffers in oxidation-reduction reactions. Plants lacking vitamin C or unusual glutathione amounts are highly sensitive to stress.

Reactive oxygen species that are protein in nature comprise of superoxide dismutase, vitamin C peroxidase, hydrogen peroxide degrading enzymes and glutathione peroxidase. Superoxide dismutase is the primary defense enzyme against reactive oxygen species. It breaks superoxide to hydrogen peroxide. Vitamin C peroxidase, glutathione peroxidase, and hydrogen peroxide degrading enzymes the detoxify hydrogen peroxide. The plant genes contains information for iso-forms of superoxide dismutase and vitamin C peroxidase and are strictly aimed for chlorophyll containing organelle, the plant power houses, peroxisomes and cytoplasm.


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