[Decarboxylation of L-methionine by Proteus vulgaris and Bacillus sphaericus].
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Ascomycota↗
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Utilization of nitrogen compounds and ammonia assimilation by Chromatiaceae.
Chromatium vinosum strain D, Thiocapsa roseopersicina strain 6311 and Ectothiorhodospira mobilis strain 8112 were grown anaerobically in the light with various single nitrogen sources. When substituted for NH4Cl only glutamine and casamino acids supported good growth of all strains tested. Peptone and urea were utilized by C. vinosum and T. roseopersicina, glutamate, asparagine and nitrate only by C. vinosum. The strains were able to grow with molecular nitrogen; complete inhibition of this growth was observed in the presence of alanine with E. mobilis, and of alanine or asparagine with T. roseopersicina. Glutamate dehydrogenase, requiring either NADH or NADPH, NADH-linked glutamate synthase, and glutamine synthetase were demonstrated in the above organisms grown on NH4Cl.
Amino Acids↗
Red blood cell anti-oxidant parameters in silicosis.
The anti-oxidant phenotype was determined in red blood cells and plasma of a group of male control subjects (n = 48) and a number of silicosis patients (n = 19). Haemoglobin, reduced and oxidized glutathione, glutathione peroxidase and superoxide dismutase were determined in red blood cells after haemolysis. In plasma, water soluble fluorescent substances were determined as a measure of in vivo lipid peroxidation. A significant increase in red blood cell glutathione was observed in silicosis patients. Moreover, some factors of the anti-oxidant system are strongly correlated in the diseased, but not in the healthy subjects. We hypothesize that individual susceptibility differences towards the development of silicosis after prolonged inhalation of silica is associated with a genetically controlled anti-oxidant phenotype.
Aged↗
High-dose combination cyclophosphamide, cisplatin, and melphalan with autologous bone marrow support. A clinical and pharmacologic study.
A total of 23 patients were treated at five dose escalations with high-dose combination cyclophosphamide, cisplatin, and melphalan with autologous bone marrow support. The maximum tolerated doses of cyclophosphamide, cisplatin, and melphalan were 5,625, 180, and 80 mg/m2, respectively. The dose-limiting toxicity was cardiac toxicity. Objective tumor regression occurred in 14 of 18 evaluable cases, with a median duration of 3.5 months. Pharmacokinetic evaluation of melphalan in 20 patients revealed a dose-related increase in maximum plasma concentration (Cmax) and area under the curve (AUC). Perturbation of the melphalan plasma half-life and AUC, associated with severe toxicity, resulted when renal insufficiency occurred. The results suggest that high-dose combination cyclophosphamide, cisplatin, and melphalan produces frequent, rapid responses in breast cancer, melanoma, and sarcoma, although with significant extramedullary toxicity. The pharmacokinetics suggest that modification of the treatment schedule may result in a reduction of treatment-related toxicity.
Adult↗
Evidence for lipid peroxidation during the calcium paradox in vitamin E-deficient rat heart.
Vitamin E is known to play an important role in the protective capacity of tissues as a free radical scavenger. Rats were made deficient in vitamin E, in order to demonstrate more clearly the formation of free radicals after exposing the rat heart to sudden changes in calcium homeostasis. The formation of malondialdehyde was taken as measure for lipid peroxidation. Malondialdehyde was detected in appreciable amounts both in heart tissue and coronary perfusate of vitamin E-deficient rat hearts after exposing them to the sudden changes in calcium concentration as seen during the calcium paradox. These findings emphasize a the hearts of normally fed rats no malondialdehyde could be detected in tissue or coronary perfusate after the calcium paradox. Therefore an essential role for vitamin E against oxidative stress in heart tissue is also indicated.
Animals↗
[Biosynthesis of volatile amines by an amine transaminase in flowering plants].
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Acetaldehyde↗
Analysis and pharmacokinetics of N-l-leucyldoxorubucin and metabolites in tissues of tumor-bearing BALB/c mice.
Leucyldoxorubicin (Leu-Dox) was developed as a prodrug of doxorubicin (Dox) with the aim of lowering the cardiotoxicity and improving the therapeutic index produced by Dox. To support the preclinical findings on its antitumor activity and cardiotoxicity, concentrations of Leu-Dox and its metabolites were determined in plasma, heart, and tumor after the administration of Leu-Dox to tumor-bearing mice. A liquid-liquid extraction procedure employing a chloroform/2-propanol/dimethylsulfoxide (DMSO) mixture was developed. By means of high-performance liquid chromatography (HPLC) with fluorescence detection, Leu-Dox and six of its metabolites could be assayed in the tissues with high sensitivity. Detection limits ranged from 0.01 nmol/g tissue for the aglycons to 0.06 nmol/g for Dox. Recoveries were in the range of 82%-110%, and calibration curves were linear over the concentration range tested (0.1-10 nmol/g tissue, r > or = 0.998). Concentration versus time curves were constructed for plasma, heart, and tumor over the first 72 h, and areas under the curves (AUCs) for the first 48 h were determined by the trapezoidal rule. Dox was rapidly formed from Leu-Dox, reaching peak levels in plasma within 5 min and in tissues within 1 h after i.v. administration of Leu-Dox (12 mg/kg). The elimination of Leu-Dox was also fast as illustrated by final half-lives of 1.1, 0.8, and 0.9 h in the plasma, heart, and tumor, respectively. For Dox, the final half-lives were 16.7 h in plasma, 15.3 h in heart tissues, and 27.4 h in tumor tissues. AUC values determined for Leu-Dox and Dox were 221 and 51 nmol ml-1 min, 443 and 4,262 nmol g-1 min, and 153 and 1,466 nmol g-1 min in the plasma, heart, and tumor, respectively. Comparison of these values with those obtained after an equimolar dose of Dox indicated 26%, 30%, and 16% of Leu-Dox appeared as Dox in the plasma, heart, and tumor, respectively. Thus, not only is the plasma compartment not representative for calculations of the conversion of Leu-Dox into Dox in tissue, but differences in its appearance also exist between the tissue compartments. The AUC values found for Dox in the heart may explain the reduced cardiotoxicity elicited by Leu-Dox as compared with Dox; however, the values obtained for Dox in the insensitive murine colon tumor cannot explain the enhanced antitumor activity exerted by Leu-Dox in the sensitive human tumor xenografts in nude mice.
Animals↗
Modulation of the in vitro cardiotoxicity of doxorubicin by flavonoids.
Cancer therapy with the anthracycline doxorubicin (Dox) is limited by cardiomyopathy, which develops in animals and patients after cumulative dosing. Generation of free radicals by Dox may be involved in this cardiotoxicity. Dox binds strongly to metal ions, especially iron(III). This Dox-metal complex stimulates the generation of free radicals through self-reduction of the complex. We investigated the possibility of inhibiting Dox-induced cardiotoxicity by scavenging of free radicals and/or chelating metal ions. The effects of Dox, both alone and in combination with iron-chelating agents, were studied on inotropy of the isolated mouse left atrium, lipid peroxidation (LPO) in cardiac microsomal membranes, ferricytochrome c (cyt.c3+) reduction, and oxygen consumption. The flavonoids 7-monohydroxyethylrutoside (mono-HER) and 7,3',4'-trihydroxyethylrutoside (tri-HER) and the ethylenediaminetetraacetic acid (EDTA) analogue ICRF-198 and its precursor ICRF-187 were used as iron-chelating agents. The latter were used for comparison since ICRF-187 has been reported to inhibit the cardiotoxic effects of Dox both in vitro and in vivo. Only the flavonoids could inhibit the negative inotropic effect of Dox (35 microM) on the mouse left atrium; in the presence of tri-HER (500 microM) the beating force decreased by 18% instead of 50%, whereas mono-HER completely prevented the Dox-induced negative inotropic effect. ICRF-198 and both flavonoids (500 microM) completely inhibited Dox (35 microM)-induced LPO, whereas ICRF-187 provided 65% inhibition. The observation that both cyt.c3+ reduction and oxygen consumption induced by the Dox-iron(III) complex (50/16.6 microM Dox3Fe3+) could be inhibited by superoxide dismutase proved the involvement of superoxide anions (O2-.). The iron-chelating agents (50 microM) inhibited cyt.c3+ reduction by 91% (mono-HER), 43% (tri-HER), and 100% (ICRF-198). Only mono-HER and ICRF-198 (50 microM) were capable of inhibiting the oxygen consumption by 70% and 43%, respectively. It is concluded that flavonoids offer a good perspective for further studies on the prevention of Dox-induced cardiomyopathy.
Animals↗
Prevention of cigarette smoking in seventh grade students.
An 8-month school-based smoking prevention program tested with 1526 seventh grade students resulted in a substantial reduction in the incidence of smoking relative to a comparison population. Two curriculum elements were found to have important deterrent effects on smoking onset: (1) emphasis on immediate and primarily social consequences of smoking and (2) personalization of the course materials and mode of presentation to include relevant peer role models and active individual role playing. Thiocyanate analysis of saliva samples taken from all participants corroborated the validity of self-report measures of smoking behavior.
Adolescent↗
Identification of beta 2-adrenoceptors on guinea pig alveolar macrophages using (-)-3-[125I]iodocyanopindolol.
The beta-adrenoceptor antagonist (-)-3-[125I]iodocyanopindolol ([125I]ICYP) binds with high affinity and in saturable way to membranes of guinea pig alveolar macrophages. The equilibrium dissociation constant for [125I]ICYP is 24.3 +/- 1.2 pM, and the number of binding sites is 166.3 +/- 13.7 fmol/mg protein (N = 4, +/- SEM). Displacement studies with selective antagonists showed that [125I]ICYP labels beta 2-adrenoceptors on guinea pig alveolar macrophages.
Adrenergic beta-Antagonists↗
Effect of multiple administration of orphenadrine or mono-N-desmethylorphenadrine on cytochrome P-450 catalyzed reactions in the rat.
Multiple administration (i.p.) of orphenadrine or its mono-N-demethylated metabolite, tofenacine (day 1, 20 mg/kg; day 2-5, 30 mg/kg) results in a considerable induction (50%) of the total cytochrome P-450 content. In addition, approximately 6% of the total amount of cytochrome P-450 was found to be blocked by a metabolic intermediate, formed from orphenadrine or tofenacine. Induction is apparent in enhancing the in vitro N-demethylation of aminopyrine and ethylmorphine and the p-hydroxylation of aniline. Pretreatment induced orphenadrine metabolism in vitro. The metabolism of tofenacine, however, was reduced. Probably this is due to a specific inhibition caused by the irreversible interaction of the metabolic intermediate with cytochrome P-450. In vivo, no induction of the aminopyrine metabolism (30 mg/kg, i.v.) is apparent, i.e., no change in the clearance was observed after pretreatment. This is probably due to the presence of relatively high, inhibitory concentrations of tofenacine (in the vicinity of cytochrome P-450). These results show that during chronic administration of orphenadrine or tofenacine, the in vivo disposition of concomitantly ingested compounds is determined by the influence of induction, high substrate and/or metabolite levels and complexation of cytochrome P-450. Moreover, based on these results an hypothesis is put forward in order to explain the phenomenon of product inhibition, which has been suggested to occur in man under chronic orphenadrine dosing conditions.
Aminopyrine↗
The repair of bone and fate of autogenous bone grafts in the skull.
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Bone Transplantation↗
Unprimed CD4+ and CD8+ T cells can be rapidly activated by a CD3 x CD19 bispecific antibody to proliferate and become cytotoxic.
We previously reported that a CD3 x CD19 bispecific antibody (bsAb) can induce efficient killing of tumour cells by preactivated T cells isolated from patients with B cell malignancy. For future intravenous application we investigated whether resting T cells from peripheral blood can be stimulated to proliferate and become cytotoxic with the CD3 x CD19 bsAb alone. Indeed peripheral blood mononuclear cells, isolated from healthy donors or patients with B cell malignancy, started to proliferate within 1 day in response to CD3 x CD19 bsAb. Within the same time span cytotoxic activity against CD19-positive tumour cells was already detectable. Maintenance of cytotoxic activity was seen during 3 days of culture but optimal lysis of the target cells then required fresh CD3 x CD19 bsAb in the cytotoxicity assay. Essentially the same results for proliferation and cytotoxicity were found when separated CD4-positive and CD8-positive T cells were activated by the bsAb in the presence of autologous monocytes. These results may be relevant for the in vivo application of the bsAb when used as immunotherapy in patients with B cell malignancy.
Antibodies, Bispecific↗
The effect of histamine on the oxidative burst of HL60 cells before and after exposure to reactive oxygen species.
During an inflammation neutrophils are stimulated to produce reactive oxygen species (ROS). These ROS induce the release of histamine from mast cells, which are also present at the inflammation site. In this study dibutyryl cAMP differentiated HL60 cells are used as a model for human neutrophils. The effect of histamine on formyl-methionyl-leucyl-phenylalanine (fmlp) stimulated cells is examined. Except for histamine also an accumulation of ROS takes place at the inflammation site and we investigated if ROS can influence the response of the stimulated HL60 cells. It is found that 10(-3) M histamine can inhibit the fmlp induced superoxide anion radical production. This occurs partly via an H2 receptor because H2 antagonists like famotidine, mifentidine and ranitidine could partially antagonize this effect of histamine. When HL60 cells are exposed to hydrogen peroxide or hypochlorous acid (20 min), an increased fmlp response is found while the inhibiting effect of histamine remains unchanged.
Bucladesine↗
Immunocytochemical detection of breast cancer cells in marrow and peripheral blood of patients undergoing high dose chemotherapy with autologous stem cell support.
Detection of small numbers of breast cancer cells is important in staging the disease and can be helpful in assessing the efficacy of purging regimens prior to autologous stem cell infusion. Immunohistochemical methods are potentially useful and broadly applicable for this purpose since they are simple to perform, sensitive, and may be quite specific. We have used a combination of four monoclonal antibodies [260F9, 520C9, 317G5 (Baxter Corp); BrE-3 (Dr. R. Ceriani)] against tumor cell surface glycoproteins in a sensitive immunocytochemical assay to identify breast tumor cells in bone marrow and peripheral blood. Immunostained cytospin preparations were fixed prior to staining to preserve cytological details of immunopositive cells. After immunostaining, slides were counterstained with hematoxylin to confirm the identify of labeled cells. In cytocentrifuge experiments in which small numbers of CAMA human breast tumor cells were added to bone marrow mononuclear cells, a linear relationship between the number of tumor cells added and the number of tumor cells detected was obtained over a broad range of tumor cell concentrations. The probability of detecting tumor cells was dependent on the number of cytocentrifuge slides examined. When ten slides (5 million cells) were examined, the probability of detecting tumor at a concentration of 4 tumor cells per million bone marrow mononuclear cells was 98%. In clinical specimens, tumor cells were detected in marrow aspirates from 73 of 240 (30%) patients undergoing autologous transplantation, including 70 (37%) of 190 patients with clinical stage IV disease, 0 of 7 patients with clinical stage III disease, and 3 of 43 (7%) patients with clinical stage II disease. Seventy-three of 657 peripheral blood specimens from 26 of 155 patients (17%) contained breast cancer cells with counts ranging from 1 to 97 tumor cells per million leukocytes. Tumor cells were most frequently found in the blood of patients with stage IV disease [21 of 107 (20%)] but were also found in a substantial number [5 of 44 (11%)] of patients with stage II disease. Positive selection of CD34-positive hematopoietic progenitor cells as well as negative purging methods such as incubation with 4-hydroxyperoxy-cyclophosphamide (4-HC) were evaluated with respect to tumor cell depletion. Selection of CD34-positive progenitor cells from bone marrow or peripheral blood resulted in log reduction of 1 to > 4 tumor cells reinfused at autologous transplantation. A lesser log reduction (up to 1) was demonstrated following 4-HC purging. We conclude that properly performed and controlled immunocytochemical staining of bone marrow and peripheral blood cytospins is a sensitive and simple way to detect and quantitate breast cancer cells in hematopoietic specimens harvested for autotransplantation and that CD34-positive progenitor cell selection results in significant reduction in the number of breast cancer cells reinfused with marrow or peripheral blood stem cells.
Antibodies, Monoclonal↗
Hydroxyl radicals are not involved in NADPH dependent microsomal lipid peroxidation.
NADPH dependent H2O2 formation in microsomes in the presence of chelated iron leads to formation of hydroxyl radicals. Enhancement of hydroxyl radical generation (via ferric-EDTA or sodium azide) did not result in a concomitant increase in lipid peroxidation; rather, a decrease was observed. Moreover, the hydroxyl radical scavenger DMSO did not inhibit lipid peroxidation. This comparison of hydroxyl radical formation with lipid peroxidation suggests that hydroxyl radicals do not play a part in NADPH-dependent lipid peroxidation.
Animals↗
Oxidative stress. Biochemistry and human disease.
The early involvement of free radicals in the evolution of life may explain their ubiquitous presence and vital physiological role. Imbalance between protection against free radicals and their generation, explains the likely association of various diseases with toxic oxygen species. An elaborate defence system against oxygen-free radicals exists. The effects of oxidative stress are manifold. Direct demonstration of oxygen radicals in intact biological systems is difficult. Frequently, effect-related measurements are used in this respect. The clinical conditions adult respiratory distress syndrome and multiple organ failure, reflex sympathetic dystrophy and sugar cataract are discussed and the role of oxygen radicals in the aetiology of these diseases are described.
Free Radicals↗
The effects of beta-adrenergic receptor agonists on the H2O2 formation in alveolar macrophage suspensions are not mediated by beta-receptors.
In the present study, the effects of beta-adrenergic receptor agonists on the hydrogen peroxide (H2O2) production in phorbol myristate acetate stimulated guinea pig alveolar macrophage suspensions have been investigated. In contrast to suggestions described in literature, our results indicate that the H2O2 production in alveolar macrophage suspensions is not mediated by beta-adrenergic receptors. Rather, it is suggested that the inhibitory effect of catecholamines in the H2O2 formation which is found after 5 minutes is the result of inhibition of the horseradish peroxidase catalysed phenol red oxidation, used as H2O2 measurement, by the catecholamines.
Adrenergic beta-Agonists↗