234 P. BISWAS ET AL.
et al. 2005). The original hypothesis was proposed by Lyons (1973).
The proposed “membrane theory” postulated that lipid phase transi-
tion in cell membranes during chilling exposure constitutes the pri-
mary response of this physiological disorder and ultimately causes
molecular and structural alteration in the lipid matrix. The sustained
primary damage then leads to a cascade of secondary events that
are reflected in tissue damage, including metabolic dysfunction, ionic
imbalances, altered metabolism, reduced photosynthesis, accumula-
tion of toxic compounds, altered enzyme activities, and the loss of
membrane integrity that leads to visible symptoms of chilling injury
(Raison and Orr 1990). The resulting symptoms are loss of turgor,
ion/water leakage, altered ripening, pitting, and loss of product qual-
ity such as flavor loss (Marangoni et al. 1996; Valdenegro et al. 2005).
- Role of Lipid Composition in Cell Membranes. Plasma membranes
consist of about 80% lipids and proteins, the remaining 20% being car-
bohydrates. Phospholipids, the most abundant membrane lipid, con-
tain a charged hydrophilic head group that interacts with the external
aqueous environment, and two hydrophobic fatty acid tails that interact
with each other. These lipid molecules associate with proteins to form
a bilayer that is fluid in normal physiological conditions above chilling
temperatures (Staehelin and Newcomb 2000).
The fluidity of the cell membrane is essential for normal membrane
function, and is believed to be important for its resistance and adapta-
tion to various physiological stresses, including low temperature (Lurie
et al. 1995). Lyons (1973) suggested that as chilling-sensitive crops are
exposed to low temperatures, there is a general increase in the micro-
viscosity of the lipid matrix due to a reduction of random rotation
or flip-flop of phospholipids and a decreased mobility of unsaturated
fatty acids. Some of the normally fluid components thus become semi-
crystalline or solid gel state (Raison and Orr 1990). This phase transi-
tion of liquid to gel-like state is affected by the nature of the lipids and
the ionic strength of cell contents and both gel and liquid phases can
coexist (Freedman 1981). The rigid gel structure may cause loss of mem-
brane elasticity and dysfunction of membrane proteins (Sevillano et al.
2009). Eventually, this may lead to cell membrane rupture, membranes
becoming leaky to electrolytes, and diminishing ion gradients across
the membranes that are essential for physiological activities of the cell
(Murata and Nishida 1990).
The membrane fluidity in a tissue is greatly affected by the fatty acid
composition of the phospholipids and interactions with other mem-
brane components (Staehelin and Newcomb 2000). Decrease in the