Cell membranes form the outer boundary of every living cell, regulating the passage of substances in and out. These flexible, constantly moving structures are essential for cell function. Their state is sensitive to temperature, which impacts their integrity. Membrane fluidity is linked to cellular processes, making stability under changing temperatures important for cell survival.
The Nature of Cell Membranes and Temperature
Cell membranes are described by the fluid mosaic model, depicting them as a fluid lipid bilayer with embedded proteins. This bilayer is primarily composed of phospholipid molecules, each with a hydrophilic head and two hydrophobic fatty acid tails. They arrange into a double layer, tails facing inward, forming a barrier between the cell’s interior and exterior. The “fluid” aspect refers to the constant movement of lipids and proteins, allowing flexibility and dynamic functions.
Membrane fluidity is directly influenced by temperature. At warmer temperatures, phospholipids have more kinetic energy, leading to increased movement and a fluid, liquid-crystalline state. As temperatures drop, kinetic energy decreases, causing them to pack closely. This leads to a phase transition, shifting the membrane from fluid to a rigid, gel-like phase. This transition temperature (Tm) varies with lipid composition, influenced by fatty acid chain length and saturation.
How Freezing Impacts Cell Membranes
Freezing temperatures can damage cell membranes through several mechanisms. Ice crystal formation is a primary issue. Extracellular ice, forming outside the cell, draws water out through osmosis, causing dehydration. This causes the cell to shrink, increasing solute concentration.
If cooling is too rapid, intracellular ice crystals can form. These internal crystals puncture and rupture the membrane, causing damage. The formation of ice, whether inside or outside the cell, disrupts the membrane’s integrity.
As temperatures fall, the membrane becomes rigid, entering a gel phase. This rigidity compromises membrane function, affecting embedded proteins that facilitate transport and signaling. A rigid state can lead to changes in permeability, making it leaky and unable to maintain separation between the cell’s interior and exterior.
Upon thawing, this loss of integrity can rupture the membrane, spilling contents and causing cell death. Rapid water influx or efflux during freezing and thawing also creates osmotic stress, contributing to membrane damage.
Protecting Membranes from Freezing Damage
Organisms in cold environments have evolved strategies to protect their cell membranes from freezing damage. Some fish and insects produce antifreeze proteins, which bind to ice crystals and prevent their growth. Other organisms, like amphibians, accumulate natural cryoprotectants such as glycerol or glucose. These compounds act as “antifreeze” by lowering the freezing point of intracellular fluid and reducing ice formation. Some species also use controlled dehydration, removing water from cells to reduce intracellular ice formation.
These natural adaptations have inspired cryopreservation techniques for preserving cells, tissues, and organs. Synthetic cryoprotective agents (CPAs), such as dimethyl sulfoxide (DMSO) and ethylene glycol, are commonly used. These agents penetrate cells, lowering the freezing point and vitrifying intracellular water, meaning it solidifies into a glass-like state without forming destructive ice crystals. Vitrification is an effective strategy as it avoids ice crystal formation.
Controlled cooling and warming rates are also important in cryopreservation protocols. Slow cooling allows water to move out of cells, minimizing intracellular ice. Controlled warming prevents larger ice crystals during thawing, a process known as recrystallization. These methods are important for successful preservation in fields such as organ banking, fertility treatments, and cell line preservation for research. Protecting membranes from freezing damage has implications for medicine and scientific advancement.