The microviscosity of artificial
lipid membranes and natural membranes was measured by the fluorescence polarization technique employing
perylene as the probe.
Lipid dispersions composed of brain
gangliosides exhibited greater microviscosity than
phosphatidylserine (268 cP vs 173 cP, at 25 degrees C). Incorporation of
cholesterol (30-50%) increased the microviscosity of
lipid phases by 200-500 cP.
Cholesterol's effect on membrane fluidity was completely reversed by
digitonin but not by
amphotericin B. Incorporation of
membrane proteins into
lipid vesicles gave varying results.
Cytochrome b5 did not alter membrane fluidity. However, myelin proteolipid produced an apparent increase in microviscosity, but this effect might be due to partitioning of
perylene between
lipid and protein binding sites since tha latter have a higher fluorescence anisotropy than the
lipid. The
local anesthetics tetracain and
butacaine increased the fluidity of
lipid dispersions, natural membranes and intact
ascites tumor cell membranes. The effect of
anesthetics appears to be due to an increased disordering of
lipid structure. The fluidity of natural membranes at 25 degrees C varied as follows: polymorphonuclear leukocytes, 335 cP; bovine brain myelin, 270 cP; human erythrocyte, 180 cP; rat liver microsomes, 95 cP; rat liver mitochondria, 90 cP. In most cases the microviscosity of natural membranes reflects their
cholesterol:
phospholipid ratio. The natural variations in fluidity of cellular membranes probably reflect important functional requirements. Similarly, the effects of some drugs which alter membrane permeability may be the result of their effects on membrane fluidity.