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Biomedical subjects

R Docampo

Publications and source records attributed to R Docampo.

At least 19 recordsLinked to original sources
PubMed1979

Acetate oxidation by bloodstream forms of Trypanosoma cruzi.

Bloodstream forms of Trypanosoma cruzi had a substantial increase in respiration in the presence of acetate. Oxidation of acetate took place via the tricarboxylic acid cycle and involved an antimycin A-sensitive respiratory pathway. Oxygen uptake in the presence of acetate was a sensitive to antimycin A inhibition as was CO2 production. There was a 6--7% residual O2 uptake which was not inhibited by high antimycin concentrations. Human anti-T. cruzi sera had no effect on oxygen uptake.

Acetates↗
PubMed1978

Ultrastructural alterations and peroxide formation induced by naphthoquinones in different stages of Trypanosoma cruzi.

Addition of beta-lapachone, an o-naphthoquinone with bactericidal, cytotoxic, and trypanocidal activities, to Trypanosoma cruzi epimastigote and amastigote stages induced the release of O2- and H2O2 from the whole cells into the suspending medium. In the presence of reduced nicotinamide adenine dinucleotide as reductant beta-lapachone was also able to stimulate O2- and H2O2 production by homogenates of these stages. Electron micrographs showed that in beta-lapachone-treated amastigotes and trypomastigotes, the chromatin is arranged in patches, clearly differing from the normal pattern of chromatin distribution. Alterations of the nuclear, mitochondrial, and cytoplasmic membranes, as well as swelling of the mitochondria were also observed.

Animals↗
PubMed1978

Effect of beta-lapachone on superoxide anion and hydrogen peroxide production in Trypanosoma cruzi.

Addition of beta-lapachone, an o-naphthoquinone endowed with trypanocidal properties to respiring Trypanosoma cruzi epimastigotes induced the release of O2- and H2O2 from the whole cells to the suspending medium. The same beta-lapachone concentration (4 micron) that released H2O2 at maximal rate completely inhibited T. cruzi growth in a liquid medium. The position isomer, alpha-lapachone, did not stimulate O2- and H2O2 release, and did not inhibit epimastigote growth. beta-Lapachone was able to stimulate H2O2 production by the epimastigote homogenate in the presence of NADH as reductant. The same effect was observed with the mitochondrial fraction supplemented with NADH, where beta-lapachone enhanced the generation of O2- and H2O2 4.5- and 2.5-fold respectively. beta-Lapachone also increased O2- and H2O2 production (2.5 and 2-fold respectively) by the microsomal fraction with NADPH as reductant. Cyanide-insensitive NADH and NADPH oxidation by the mitochondrial and microsomal fractions (quinone reductase activity) was stimulated to about the same extent by beta-lapachone. alpha-Lapachone was unable to increase O2- and H2O2 production and quinone reductase activity of the mitochondrial and microsomal fractions.

Animals↗
PubMed1978

In vitro and in vivo evaluation of the toxicity of 1,4-naphthoquinone and 1,2-naphthoquinone derivatives against Trypanosoma cruzi.

The toxic effect of lapachol, beta-lapachone and several 1,2-naphthoquinone derivatives on the growth, viability and infectivity of Trypanosoma cruzi were compared. beta-lapachone was the most active compound in vitro. No inhibition was observed in suspensions which contained inactivated foetal calf serum or rabbit haemoglobin solution. The infectivity of trypomastigotes in mice was not affected when cells were previously incubated with beta-lapachone or one of several other naphthoquinone derivatives in vitro in the presence of blood. It is suggested that beta-lapachone and the other compounds can be inactivated either by reduction in the presence of oxyhaemoglobin or by interaction with serum proteins. A beta-lapachone derivative, allyl-beta-lapachone, was not inactivated in the presence of blood and remained effective in suppressing trypomastigote infectivity.

Animals↗
PubMed1978

Generation of free radicals from phenazine methosulfate in Trypanosoma cruzi epimastigotes.

A significant growth inhibition of Trypanosoma cruzi epimastigotes by phenazine methosulfate (PMS) was observed in Warren's medium. This toxic activity could be related to the following parameters: a) formation of phenazinium free radical, b) generation of superoxide anion in intact cells incubated with PMS, and c) PMS also increased significantly the rate of O2- generation in epimastigotes mitochondrial and microsomal fractions using NADH as electron donor.

Electron Spin Resonance Spectroscopy↗
PubMed1976

Localization of peroxidase activity in Trypanosoma cruzi microbodies.

Electron microscopic observation of Trypanosoma cruzi epimastigotes reveals the presence of microbody-like structures (microperoxisomes) in which 3,3'-diaminobenzidine (DAB) is peroxidized to electron-opaque material. The role of peroxidase in DAB peroxidation is supported by the enzyme demonstration in disrupted epimastigotes and the microbody-containing cell fractions.

Animals↗