Lipid content of the slender and stumpy forms of Trypanosoma brucei rhodesiense: A comparative study

Venkatesan, S.; Ormerod, W.E.

doi:10.1016/0305-0491(76)90203-0

Cited by 20 publications

(11 citation statements)

References 33 publications

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“…2 A, live trypanosomes secreted small amounts of PGs: 75 ± 10 pg/ml for PGD 2 , 100 ± 9.4 pg/ml for PGE 2 , and 156 ± 20 pg/ml for PGF 2α ( n = 3). As with other parasitic protozoa, T. brucei does not synthesize AA de novo from acetate 29, but it does take up this fatty acid from its environment and does incorporate it into its total and separate classes of lipids 3031. The presence of phospholipase A 2 3233, an enzyme that catalyzes the release of AA from phospholipids, in T. brucei indicates the existence of a free intracellular AA source in this parasitic protozoan.…”

Section: Resultsmentioning

confidence: 98%

Identification of a Novel Prostaglandin F2α Synthase in Trypanosoma brucei

Kubata¹,

Duszenko

Kabututu

et al. 2000

The Journal of Experimental Medicine

101

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Members of the genus Trypanosoma cause African trypanosomiasis in humans and animals in Africa. Infection of mammals by African trypanosomes is characterized by an upregulation of prostaglandin (PG) production in the plasma and cerebrospinal fluid. These metabolites of arachidonic acid (AA) may, in part, be responsible for symptoms such as fever, headache, immunosuppression, deep muscle hyperaesthesia, miscarriage, ovarian dysfunction, sleepiness, and other symptoms observed in patients with chronic African trypanosomiasis. Here, we show that the protozoan parasite T. brucei is involved in PG production and that it produces PGs enzymatically from AA and its metabolite, PGH2. Among all PGs synthesized, PGF2α was the major prostanoid produced by trypanosome lysates. We have purified a novel T. brucei PGF2α synthase (TbPGFS) and cloned its cDNA. Phylogenetic analysis and molecular properties revealed that TbPGFS is completely distinct from mammalian PGF synthases. We also found that TbPGFS mRNA expression and TbPGFS activity were high in the early logarithmic growth phase and low during the stationary phase. The characterization of TbPGFS and its gene in T. brucei provides a basis for the molecular analysis of the role of parasite-derived PGF2α in the physiology of the parasite and the pathogenesis of African trypanosomiasis.

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Section: Resultsmentioning

confidence: 98%

Identification of a Novel Prostaglandin F2α Synthase in Trypanosoma brucei

Kubata¹,

Duszenko

Kabututu

et al. 2000

The Journal of Experimental Medicine

101

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“…Lipids including triacyglycerols, phospholipids, plasmalogens, sterols, and isoprenoids (19,39,40,124,135) constitute 15%-20% of the dry weight of African trypanosomes (124). Sterols are particularly important for these parasites, not only to stabilize biological membranes but also to prevent temperature-induced phase transition, a crucial feature for parasites shuttling between homeotherm and poikilotherm hosts.…”

Section: Role Of Low-density Lipoprotein Receptor In Lipid Importmentioning

confidence: 99%

The Adaptative Mechanisms ofTrypanosoma Bruceifor Sterol Homeostasis in Its Different Life-Cycle Environments

Coppens

Courtoy

2000

Annu. Rev. Microbiol.

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Bloodstream forms of Trypanosoma brucei do not synthesize sterols de novo and therefore cannot survive in medium devoid of lipoproteins. Growth of parasites is essentially supported by receptor-mediated endocytosis of low-density lipoproteins (LDLs), which carry phospholipids and cholesteryl esters. These lipids are released from internalized LDL after apoprotein B-100 is degraded by acidic thiol-proteases in the endolysosomal apparatus and then metabolized, as in mammalian cells. The LDL receptor is recycled and its expression is regulated by the sterol stores. Documented pharmacological and immunological interferences with LDL receptor-mediated lipid supply to the bloodstream forms are summarized, and the potential for new approaches to fight against these parasites is evaluated. In contrast to bloodstream forms, cultured procyclic forms can acquire sterols from both exogenous (lipoprotein endocytosis) and endogenous (biosynthesis of ergosterol) sources. The rate-limiting steps of both endocytosis (surface LDL receptor expression) and biosynthesis (3-hydroxy-3-methylglutaryl coenzyme A reductase activity) are regulated by the cellular content of sterol. These two pathways thus complement each other to yield a balanced sterol supply, which demonstrates adaptative capacities to survive in totally different environments and fine regulatory mechanisms of sterol homeostasis.

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“…32 The bands were visualized with iodine. Those corresponding to unesterified fatty acids, triacylglycerols, and cholesteryl esters were scraped off, and the fatty acids were methylated or transmethylated with boron trifluoride at 85°C to 90°C for 20 minutes.…”

Section: Concentration and Composition Of Fatty Acidsmentioning

confidence: 99%

Dietary fat induces changes in factor VII coagulant activity through effects on plasma free stearic acid concentration.

Mitropoulos

Miller

Martin

et al. 1994

Arterioscler Thromb

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Previous studies have demonstrated activation of the contact system of coagulation and an increase in factor VII coagulant activity (VIIc) when citrated plasma is incubated in the presence of micellar stearate. The products of contact activation, factors Xlla and IXa, were responsible in this system for the activation of factor VII, thereby increasing factor VIIc. To obtain evidence that these in vitro interactions also operate in vivo, factor VIIc was examined in relation to plasma free fatty acid concentrations in five healthy individuals during the consumption of isocaloric high-saturated fat, high-unsaturated fat, and low-fat diets, each taken for 4 weeks in random order and separated by intervals of 12 weeks. For all but the final 3 days of each phase, subjects selected appropriate foods from prepared lists to meet the dietary requirements. Experimental diets of predetermined fat content and composition were fed on days 26 through 28 in each phase. Fat supplied on average 62% of energy in two of the experimental diets and less than 20% of energy in the third. On the final day of each dietary phase, the concentrations of the various free fatty acids and factor VIIc were measured before breakfast and at three 150-minute intervals thereafter. Plasma factor VIIc was, respectively, 6.5% and 13.1% of standard higher on the unsaturated and saturated fat diets than on the low-fat diet. Furthermore, the plasma concentration of stearic acid was strongly associated with factor VIIc (r=.58, /><.0001), and this relation remained significant (P=.OO3) after allowance for the plasma concentrations of palmitic, oleic, and linoleic acids. Plasma factor VII antigen levels were increased on the saturated fat diet but were very similar on the other two diets. These results suggest that the effects of saturated fatty acids observed in vitro on factor VIIc also operate in vivo. (Arterioscler Thromb. 1994;14:214-222

show abstract

Lipid content of the slender and stumpy forms of Trypanosoma brucei rhodesiense: A comparative study

Cited by 20 publications

References 33 publications

Identification of a Novel Prostaglandin F2α Synthase in Trypanosoma brucei

Identification of a Novel Prostaglandin F2α Synthase in Trypanosoma brucei

The Adaptative Mechanisms ofTrypanosoma Bruceifor Sterol Homeostasis in Its Different Life-Cycle Environments

Dietary fat induces changes in factor VII coagulant activity through effects on plasma free stearic acid concentration.

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