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Biomedical subjects

F S Cruz

Publications and source records attributed to F S Cruz.

14 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

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

Chemically defined media for growing anaerobic bacteria of the genus Veillonella.

A chemically defined medium for Veillonella parvula and V. alcalescens is described. Some nutritional aspects of the two strains used were examined: the optimum concentration of reducing agents, the requirements for amino acids, diamines, vitamins and other growth factors, and the conditions needed for well balanced nutrition. No specific requirements for single amino acids were observed. A combination of L-cysteine, DL-aspartic acid, L-glutamic acid, L-serine and L-tyrosine, promoted growth. In V. alcalescens, serine could substitute both arginine and tryptophan (or histidine). No growth was obtained with ammonium salts as the sole N source. Decarboxylation of L-ornithine, L-lysine and L-arginine was not demonstrated in the Veillonella parvula strain, which required putrescine or cadaverine for growth. Spermine, spermidine, L-lysine, L-ornithine and L-arginine, could not substitute putrescine in Veillonella parvula. Veillonella alcalescens, which does not require putrescine in the medium, was able to decarboxylate L-ornithine while forming putrescine.

4-Aminobenzoic Acid↗
PubMed1975

Toxicity of 4-nitroquinoline 1-oxide for Crithidia fasciculata.

Growth inhibition of Crithidia fasciculata by 4-nitroquinoline 1-oxide (NQO) was observed in defined and complex media at 28 C. Aromatic amino acids, cystein, and nicotinic acid, among several other substances, were ineffective in overcoming NQO toxicity. Dicoumarol and bovine albumin reversed NQO inhibition. While bovine albumin probably acted by the extra-cellular binding of NQO, dicoumarol inhibited the activity of DT-diaphorase, which reduces NQO to 4-hydroxyaminonitroquinoline 1-oxide (HAQO). The DT-diaphorase from C. fasciculata had the same characteristics as the enzyme from rat liver. The specific protection by dicoumarol against NQO inhibition suggests that HAQO is the active toxic substance for C. fasciculata.

4-Hydroxyaminoquinoline-1-oxide↗