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Biomedical subjects

A Boveris

Publications and source records attributed to A Boveris.

At least 127 records · Page 7Linked to original sources
PubMed1980

Low-level chemiluminescence of hydroperoxide-supplemented cytochrome c.

Ferricytochrome c showed low-level chemiluminescence, with a light-emission measured of about 1x10(3)-3x10(3) counts/s, when supplemented with organic hydroperoxides. Tertiary hydroperoxides (cumene hydroperoxide and t-butyl hydroperoxide) showed a saturation behaviour at about 5mm-hydroperoxide, whereas primary hydroperoxides showed a quadratic dependence on the hydroperoxide concentration. Chemiluminescence depended linearly on cytochrome c concentration, and optimal light-emission was observed at [t-butyl hydroperoxide]/[ferricytochrome c] ratios of 160-500. Hydroperoxide-supplemented ferricytochrome c consumed O(2) at a rate of 1.0mumol/min per mumol of cytochrome c; the rate of O(2) uptake was linearly related to the concentration of cytochrome c. The Soret absorption band of ferricytochrome c decreased about 64% after incubation with t-butyl hydroperoxide, whereas the 530nm band was almost totally abolished. Light-emission was (a) inhibited competitively by cyanide. (b) inhibited by singlet-oxygen quenchers (e.g. beta-carotene), scavengers (e.g. dimethylfuran) and traps (e.g. histidine and tryptophan) and (c) increased by singlet-oxygen-chemiluminescence enhancer 1,4-diazabicyclo[2.2.2]-octane. Superoxide dismutase had no effect on the present system. The participation of free radicals is suggested by the effect of the radical trap 2,5-di-t-butylquinol. Singlet-oxygen dimol emission seems to be mainly responsible for the observed light-emission; a mechanism that can account for the major part of the present experimental observations is proposed.

Benzene Derivatives↗
PubMed1980

Low-level chemiluminescence of bovine heart submitochondrial particles.

Submitochondrial particles from bovine heart mitochondria showed low-level chemiluminescence when supplemented with organic hydroperoxides. Chemiluminescence seems to measure integratively radical reactions involved in lipid peroxidation and related processes. Maximal light-emission was about 1500 counts/s and was reached 2-10min after addition of hydroperoxides. Ethyl hydroperoxide, cumene hydroperoxide and t-butyl hydroperoxide were effective in that order. Antimycin and rotenone increased chemiluminescence by 50-60%; addition of substrates, NADH and succinate did not produce marked changes in the observed chemiluminescence. Cyanide inhibited chemiluminescence; half-maximal inhibitory effect was obtained with 0.03mm-cyanide and the inhibition was competitive with respect to t-butyl hydroperoxide. Externally added cytochrome c (10-20mum) had a marked stimulatory effect on chemiluminescence, namely a 12-fold increase in light-emission of antimycin-inhibited submitochondrial particles. Stimulation of hydroperoxide-induced chemiluminescence of submitochondrial particles by cytochrome c was matched by a burst of O(2) consumption. O(2) is believed to participate in the chain radical reactions that lead to lipid peroxidation. Superoxide anion seems to be involved in the chemiluminescence reactions as long as light-emission was 50-60% inhibitible by superoxide dismutase. Singlet-oxygen quenchers, e.g. beta-carotene and 1,4-diazabicyclo[2,2,2]-octane, affected light-emission. beta-Carotene was effective either when incorporated into the membranes or added to the cuvette. The present paper suggests that singlet molecular oxygen is mainly responsible for the light-emission in the hydroperoxide-supplemented submitochondrial particles.

Animals↗
PubMed1980

Organ chemiluminescence: noninvasive assay for oxidative radical reactions.

In situ and perfused rat livers showed a spontaneous chemiluminescence of 7-12 counts/sec . cm2 (corresponding to 7-12 x 10(3) photons/sec . cm2); chemiluminescence was increased up to 30 times by infusion of exogenous hydroperoxides. The chemiluminescence of the perfused liver was oxygen dependent. Ethyl, t-butyl, and cumene hydroperoxides were almost equally effective in inducing light emission in the perfused liver. Glutathione release and chemiluminescence showed a parallel increase upon hydroperoxide supply to the perfused liver. A partial spectral analysis of the chemiluminescence of the perfused liver showed a predominance of red-light-emitting species, presumably arising from the singlet oxygen dimol-emission peaks. Many side reactions derived from the complex free radical sequence of lipid peroxidation could afford the chemistry leading to light emission, which represents only about 10(-14) of the utilization of peroxide.

Animals↗
PubMed1979

Chemiluminescence of Acanthamoeba castellanii.

1. Chemiluminescence of Acanthomoeba castellanii in the presence of O2 was of similar intensity in organisms harvested early or late during exponential growth [when cyanide (1 mM) stimulates or inhibits respiration respectively]. 2. Cyanide (up to 1.5 mM) stimulated photoemission in both types of organism by 250--300 photons/s per 10(7) cells above the value observed under aerobic conditions. 3. 'Dibromothymoquinone' (2,5-dibromo-6-isopropyl-3-methyl-p-benzoquinone) (up to 80 microM) further increased chemiluminescence. 4. Similar responses were also demonstrated in whole homogenates and in subcellular fractions; 36% of the chemiluminescence was provided by a fraction sedimenting at 100000g-min, and 20% in that fraction that was non-sedimentable at 200000g-min. 5. Mitochondrial substrates (succinate, 2-oxoglutarate, NADH) in the presence or absence of ADP and Pi or peroxisomal substrates (glycollate, urate or ethanol) gave no increases in light emission by whole homogenates or in any of the fractions. 6. It is suggested that reactions responsible for production of chemiluminescence are those primarily producing superoxide anions and leading to lipid peroxidation and singlet-oxygen formation. Photoemission enhancement and superoxide dismutase inhibition showed similar cyanide concentration-dependencies.

Amoeba↗
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↗
PubMed1977

Hydrogen peroxide generation in Trypanosoma cruzi.

Homogenates from T. cruzi epimastigotes produced 3.4 pmoles H2O2/min 10(6) cells, as detected by the cytochrome c peroxidase assay. Addition of NADH or NADPH increased H2O2 production by a factor of 3 and 5, respectively. When supplemented with NADH and NADPH, the mitochondrial, microsomal and supernatant fractions produced H2O2, the soluble fraction and the mitochondrial membranes being apparently the main generators of H2O2. The epimastigote homogenates showed cyanide-sensitive superoxide dismutase activity, equivalent to 0.28 microgram bovine superoxide dismutase per mg homogenate protein.

Animals↗