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I.

Chilling injury symptoms in dragon fruit:


* Corrales-Garca et al. (2009):
Fruits put at 4 or 8oC for 5-21 days, transferred to 26oC for 1-6 days.
- lose ability to develop pinkish red color (hue angle does not decrease at low T)
- lose ability to increase chroma (should increase at normal T)
- lose firmness (should remain relatively constant at normal T)
- increase ethanol and acetaldehyde in pulp
- increase respiration rate
* Balois-Morales et al. (2010)

* Nerd et al. (1999):


Fruits put at 6oC for 1-3 weeks, transferred to 20oC for 1 week
- soft, high water loss, low acidity, poor flavor.
- wilting and darkening of the scales and browning of the outer layer of the pulp
* Our study:

Also: more prone to fungi? Wilting?


II. Mechanism:
1) Markhart (1986):
a. Phase transition of membrane.
- At low T, membrane fluidity is lost due to membrane lipid phase transition->
disturbance of permeability and activity of membrane enzyme (eg. transport).
- Shown by Arrhenius plot (inconsistent result). Also of activity of some membrane
enzymes.
- Depolymerization of cytoskeleton.
- Chilling-resistant plants tend to have more unsaturated fat than chilling-sensitive.
However, counter-evidence exist. -> membrane fluidity also depends on other
components: protein, carbohydrate, sterol, water (solute).
b. Abscisic acid (ABA) increase chilling tolerant
- Stress increases ABA and increase tolerance to subsequent stress.

- Not due to stamata closure.


- Maybe due to interaction with membrane, because the molecule may fit well in the
fatty acids of membrane. (Proof: broaden peak of DSC curve of lipid bilayer).
2) Parkin 1989:
- At the moment, most researchers think: CI is composed of two steps: a immediate
(primary) response due to low T, then secondary responses (physiological
response/symptoms).
- Many people look for an universal mechanism for chilling injury.
a. membrane lipid phase transition
- Basis: bulk membrane lipid phase transitions at a critical temperature resulted in
the formation of gel phase lipids. This led to increased permeability or leakiness of
cellular membranes, bringing about loss of compartmentation and regulatory
control. Ultimately, an irreversible metabolic imbalance arose and the plant
capitulated to physiological dysfunction and death.
- Mitochondria of CS plant: activity break (in Arrhenius plot) at 9-12oC, less
unsaturated acid. (Lyons et al. 1964, 1970). Not found in CR. Further biophysical
studies confirm (i.e. change in phase of membrane of mitochondria membrane at
non-freezing T).
Similar phase change of membrane and dysfunctioning found in: chloroplast,
plasma membrane (ion leakage), microsome.
-However, many critics and evidence emerge. And the theory is put in doubt.
b. membrane lipid domain
- a refinement of the lipid phase transition theory: discrete lipid domains in the
membrane may undergo a temperature- dependent increase in ordering or phase
transition (separation) below a critical temperature. -> irreversible when warming
up.

Phophatidylglycerol (PG) (a phospholipid (PL) of membrane) has more saturated


fatty acid in CS and crystallize easier than other PL.
Reasons for untrust on this theory:
+ Analysis on mitochondrial in some plants did not detect sharp decrease in activity
+ Sharp decrease in activity of mitochondria, chloroplast was also found in some CR
plants
+ Using Arrhenius plot is not accurate since respiration and photosynthesis are
complex reactions
+ Question on the accuracy of the fluorescence and probes used to detect phase
change.
+ More advances tecniques found that only a small part (5%) of lipid membrane in
CS plant undergo phase change
+ Phase change and increase in permeability only occurs after prolonged chilling,
not immediately upon chilling,
Conclusion: Only few scientists are convinced, but it is agreeable that membrane
is a primary site of injury due to low T.
Other theories:
+ Decrease of enzyme activity and disfunctioning of protein.
+ Oxidative stress due to imbalance in metabolism -> secondary response but
important to look for preventive methods.

Due to disfunctioning of mitochondria, chloroplast, ROS level increased. Also


because of increase of activity of some lipoxigenase, phosphatidase (oxidsing lipid,
inducing lipid peroxidation).
This is aggravated by decreased activity of defense mechanism like antioxidant
enzyme (SOD, CAT, Glutathione reductase).
+ Ethylene
3) Increase respiration rate -> fermentation rate -> flavor
Increase resp rate: Eaks 1960, McCollum 1991
Off flavor: Brovelli 1998, Karakurt 2000, Nair 2004 (Whitaker 2008)
Anaerobic repiration, ethanol and off flavor: Shi 2005
Biochemical and anatomical reason: Shi 2007 (Paul 2014)
4) Oxidative stress
Sevillano 2009, Lafuente 2005
Cucumber: increase of lipoxygenase and phospholipase D activity with CI (Mao 2007
a,b)
Mandarin: sensitive cultivar has lower activity of antioxidant enzyme (Sala 1998)
Heat conditioning of sensitive cultivar increase antioxidant enzyme and
chilling tolerance (Sala 1999), esp CAT
CAT inhibitor induce CI even in chilling resistant cultivar (Sala 2000).
Genetically modified with antisense for ACO (ethylene biosynthesis) reduce CI,
increase activity of antioxidant enzyme like CAT, SOD, peroxidase (Ben-Amor 1999)
-> relation of different mechanism
5) Ethylene
6) Decrease of enzyme activity
III. Current status of knowledge on chilling injury:
- All plants are chilling sensitive at the first place. Through evolution, some family or
cultivars of a species develop mechanism to increase chilling tolerance.
a. Polyamines
b. Abscisic acid
c. Heat shock protein
d. Plant growth regulator.