Serum lipoprotein and Trypanosoma brucei brucei interactions in vitro

Trypanosoma brucei brucei IL3201 and IL3202, which are dependent on serum high or low-density lipoproteins to multiply under axenic culture conditions, acquired lipoprotein-associated 3H-lipids without binding, accumulating or degrading apolipoproteins. Uptake by the T. b. brucei of lipoprotein-associated [1 alpha, 2 alpha(n)-3H]cholesterol, [1 alpha, 2 alpha(n)-3H]cholesteryl linoleate, [1 alpha, 2 alpha(n)-3H]cholesteryl oleoyl ether and L-3-phosphatidyl [N-methyl-3H]choline, 1,2-dipalmitoyl, occurred at 37 degrees C but not at 0 degree C, and tended towards saturation with increasing concentrations of 3H-lipid-labelled lipoproteins in the incubation mixture. The uptake processes did not discriminate between high- or low-density lipoproteins, did not require exogenous divalent ions and were not inhibited by the presence of acidotropic agents (chloroquine, ammonium chloride) in the incubation mixture. Uptake by T. b. brucei of lipoprotein cholesterol was likely to result mainly from desorption and diffusion processes, whereas specific binding sites were probably involved in the uptake by T. b. brucei of lipoprotein cholesteryl linoleate, cholesteryl oleoyl ether and possibly phosphatidylcholine. Exponentially growing T. b. brucei hydrolysed cholesteryl linoleate to cholesterol and had only a small capacity to reesterify cholesterol, whereas committed non-dividing stumpy form T. b. brucei had a large capacity to esterify cholesterol. Conversion products of phosphatidylcholine were generated during or after uptake of this phospholipid by exponentially growing T. b. brucei.