Temperature-Dependent Fatty Acyl Group Changes in Phospholipids of 37 C-Adapted Leishmania donovani Promastigotes

Abstract

Promastigotes of Lesihmania donovani, Stock 3S, adapted to grow in a biphasic medium at 37 C, by step-wise increases in incubation temperature from 25 C, showed marked reductions in the amounts of C8, C20, and C22 polyunsaturated fatty acyl groups present in membrane phospholipids of the 25 C-adapted flagellates. These changes may be considered a homeoviscous adaptation directed at maintenance of membrane bilayer lipids in a liquid-crystalline state appropriate to normal performance of membrane barrier functions. Such an adaptive decrease in fatty acyl groups, which contribute to lipid bilayer fluidity, argues against the concept that the adoption of an intracellular habitat by the amastigote stage of leishmanias is necessary to protect it from the consequences of temperature-induced membrane disorder and consequent loss of control of permeability. Greenblatt and Wetzel (1966), seeking a mech- anistic explanation for the responses of leish- manias to vertebrate host body temperatures, focused their attention on lipid inclusions seen earlier by Greenblatt and Glaser (1965) in Leish- mania enriettii promastigotes cultured in vitro at 25 C, then exposed to 37 C. They detected a marked increase in intracellular fatty acids and unsaponifiable lipids associated with the tem- perature shift, and attributed it to membrane lipid recycling and to conversion of endogenous metabolites to lipids. They also reported an impairment of fatty acid desaturation in the Cl8 polyunsaturated fatty acid biosynthesis pathway; stearic - oleic - linoleic - a-linolenic. The changes in lipid metabolism were thought to lead to alterations in the physical properties of mem- brane lipids, which were in turn responsible for an observed increase in the permeability of the parasite. Such an association could provide a rationale for the intracellular habitat of the amas- tigote in the warm-blooded vertebrate host. In the macrophage, the parasite might be sheltered from the consequences of altered passive mem- brane barrier properties and impaired mem- brane barrier functions (Trager, 1960). An exper- imental test of such correlations would best be