Question

Give reason why the permeability of both the membrane is same for fatty acid? ​

Answer 1

The similarity in permeability of the cell membrane for fatty acids is influenced by the fluidity of the membrane, which is determined by the nature of the phospholipid tails, with unsaturated fatty acids providing kinks that maintain fluidity even at lower temperatures.

Step-by-step explanation:

The permeability of the cell membrane for fatty acids can be similar despite the presence of both saturated and unsaturated fatty acids within the phospholipid bilayer. The key factor here is the fluidity of the membrane, which is influenced by the nature of the phospholipid tails. Saturated fatty acids have straight tails and pack tightly together, creating a more rigid membrane. Conversely, unsaturated fatty acids contain kinks or bends due to the presence of double bonds between carbon atoms, which hinders tight packing and maintains space between the molecules.

Differences in fluidity affect the way membranes respond to temperature changes. At lower temperatures, saturated fatty acids become compressed, making the membrane rigid and potentially more prone to rupture. Unsaturated fatty acids with their kinks can prevent this rigidity by maintaining fluidity even in cold environments, thereby influencing the permeability of the membrane. Thus, despite the different compositions, as long as the overall fluidity of the membrane is maintained, the permeability for fatty acids remains relatively constant.

Answer 2

Because of the amphipathicity and conical molecular shape of fatty acids.

Explanation

They can efficiently incorporate into lipid membranes and disturb membrane integrity, chain packing, and lateral pressure profile. These phenomena affect both model membranes as well as biological membranes. We investigated the feasibility of exploiting fatty acids as permeability enhancers in drug delivery systems for enhancing drug release from liposomal carriers and drug uptake by target cells. Saturated fatty acids, with acyl chain length from C8 to C20, were tested using model drug delivery liposomes of 1,2- dipalmitoyl-sn-glycerol-3-phosphocholine (DPPC) and the breast cancer MCF-7 cell line as a model cell. A calcein release assay demonstrated a reduction in the membrane permeability barrier of the DPPC, proportionally to the length of the fatty acid. Differential scanning calorimetry (DSC) and dynamic light scattering (DLS) experiments revealed that C12 to C20 fatty acids could stabilize DPPC liposomal bilayers and induce large structures, probably due to liposome aggregation and bilayer morphological changes. On the other hand, the short fatty acids C8 and C10 tend to destabilize the bilayers and only moderately cause the formation of large structures. The effect of fatty acids on DPPC liposomes was not completely transferrable to the MCF-7 cell line. Using cytotoxicity assays, the cells were relatively insensitive to the fatty acids at apoptotic sub-millimolar concentrations. Increasing the fatty acid concentration to few millimolar substantially reduced the viability of the cells, most likely via the induction of necrosis and cell lysis. A bioluminescence living-cell-based luciferase assay showed that saturated fatty acids in sub-cytotoxic concentrations could not reduce the permeability barrier of cell membranes. Our results confirm that the membrane perturbing effect of fatty acids on model membranes cannot simply be carried over to biological membranes of live cells.