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PubMed1988

Determination of coenzyme Q10, alpha-tocopherol and cholesterol in biological samples by coupled-column liquid chromatography with coulometric and ultraviolet detection.

Coenzyme (Co) Q10, Co Q10H2, alpha-tocopherol and cholesterol were dissociated from lipoproteins in plasma by treatment with 1-propanol. The supernatant obtained was injected directly for determination of Co Q10 and Co Q10H2. Precolumn reduction with borohydride was used for determination of total Co Q10 simultaneously with alpha-tocopherol and cholesterol. Total Co Q10 in freeze-dried myocardial biopsies was determined after extraction with 1-propanol and oxidation of Co Q10H2 with ferric chloride. The chromatographic system comprised two reversed-phase columns and a three-electrode coulometric detector and a UV detector coupled in series. A pre-fractionation on the first column protected the coulometric detector from contamination and reduced the time for analysis by eliminating strongly retained solutes. The coulometric electrodes were operated in the oxidation-reduction-oxidation mode, and the last electrode was used for detection of alpha-tocopherol, Co Q10 and Co Q10H2, while cholesterol was detected by UV at 215 nm. The fast isolation procedure made it possible to determine the reduced and oxidized forms of Co Q10 in plasma. Quantitative recoveries were obtained for all the analytes studied and normal levels were determined with a coefficient of variation of 2-3%.

Cholesterol↗
PubMed2001

Protein glycation: creation of catalytic sites for free radical generation.

In a glycation reaction, alpha-dicarbonyl compounds such as deoxyglucosone, methylglyoxal, and glyoxal are more reactive than the parent sugars with respect to their ability to react with amino groups of proteins to form inter- and intramolecular cross-links of proteins, stable end products called advanced Maillard products or advanced end products (AGEs). The AGEs, which are irreversibly formed, accumulate with aging, atherosclerosis, and diabetes mellitus, and are especially associated with long-lived proteins such as collagens, lens crystallins, and nerve proteins. It was suggested that the formation of AGEs not only modifies protein properites but also induces biological damage in vivo. In this report, we summerize results obtained from our studies for (1) identifying the structure of the cross-linked radical species formed in the model system-the reaction between alpha-dicarbonyl methylglyoxal with amino acids, and (2) the reactivity of the radical center of the protein created by the similar reaction. These results indicate that glycation of protein generates active centers for catalyzing one-electron oxidation-reduction reactions. This active center, which exhibits enzyme-like character, is suggested to be the cross-linked Schiff-based radical cation of the protein. It mimics the characteristics of the metal-catalyzed oxidation system. These results together indicate that glycated proteins accumulated in vivo provide stable active sites for catalyzing the formation of free redicals.

Aging↗
PubMed1999

An Interpretation of Gated Behavior: Kinetic Studies of the Oxidation and Reduction Reactions of Bis(2,9-dimethyl-1,10-phenanthroline)copper(I/II) in Acetonitrile.

Reduction reactions of Cu(dmp)(2)(2+) (dmp = 2,9-dimethyl-1,10-phenanthroline) by ferrocene (Fe(Cp)(2) = bis(cyclopentadienyl)iron(II)), decamethylferrocene (Fe(PMCp)(2) = bis(pentamethylcyclopentadienyl)iron(II)), and Co(bpy)(3)(2+) (bpy = 2,2'-bipyridine) and oxidation reactions of Cu(dmp)(2)(+) by Ni(tacn)(2)(3+) (tacn = 1,4,7-triazacyclononane) and Mn(bpyO(2))(3)(3+) (bpyO(2) = N,N'-dioxo-2,2'-bipyridine) were studied in acetonitrile for the purpose of interpreting the gated behavior involving copper(II) and -(I) species. It was shown that the electron self-exchange rate constants estimated for the Cu(dmp)(2)(2+/+) couple from the oxidation reaction of Cu(dmp)(2)(+) by Ni(tacn)(2)(3+) (5.9 x 10(2) kg mol(-)(1) s(-)(1)) and Mn(bpyO(2))(3)(3+) (2.9 x 10(4) kg mol(-)(1) s(-)(1)) were consistent with the directly measured value by NMR (5 x 10(3) kg mol(-)(1) s(-)(1)). In contrast, we obtained the electron self-exchange rate constant of Cu(dmp)(2)(2+/+) as 1.6 kg mol(-)(1) s(-)(1) from the reduction of Cu(dmp)(2)(2+) by Co(bpy)(3)(2+). The pseudo-first-order rate constant for the reduction reaction of Cu(dmp)(2)(2+) by Fe(Cp)(2) was not linear against the concentration of excess amounts of Fe(Cp)(2). A detailed analysis of the reaction revealed that the reduction of Cu(dmp)(2)(2+) involved the slow path related to the deformation of Cu(dmp)(2)(2+) (path B in Scheme 1). By using Fe(PMCp)(2) (the E degrees value is 500 mV more negative than that of Fe(Cp)(2)(+/0)) as the reductant, the mixing with another pathway involving deformation of Cu(dmp)(2)(+) (path A in Scheme 1) became more evident. The origin of the "Gated Behavior" is discussed by means of the energy differences between the "normal" and deformed Cu(II) and Cu(I) species: the difference in the crystal field activation energies corresponding to the formation of pseudo-tetrahedral Cu(II) from tetragonally distorted Cu(II) and the difference in the stabilization energies of the tetrahedral and tetragonal Cu(I) for the activation of Cu(I) species. The reduction reaction of Cu(dmp)(2)(2+) by Fe(PMCp)(2) confirmed that the mixing of the two pathways takes place by lowering the energy level corresponding to the less favorable conformational change of Cu(I) species.

Journal Article↗
PubMed2002

Regulation of human thioltransferase (hTTase) gene by AP-1 transcription factor under oxidative stress.

PURPOSE: To study the mechanism of activation of the human thioltransferase (hTTase) gene under oxidative stress. METHODS: Human lens epithelial cells (HLE-B3) were exposed to 0.1 mM H2O2 for 0, 5, 10, 15, 30, or 60 minutes; lysed; and used for gel mobility shift assay (GMSA) and supershift assay for activating protein (AP)-1 transcription factor. The search for transcriptional coactivators was performed with Western blot analysis. The ability of different parts and a mutated fragment of the hTTase gene promoter region to activate the gene expression under the oxidative stress conditions was examined by reporter gene assay. RESULTS: The AP-1-binding element was identified in the 5' region of the hTTase gene, and evidence was obtained that binding of AP-1 with this element in vivo was redox sensitive. In addition, the pattern of AP-1 binding under the oxidative stress was similar to the pattern of TTase activity and mRNA synthesis modulation. In contrast, direct exposure of the cell lysate to oxidants, reductants, or redox-regulating enzymes in vitro had no influence on AP-1 binding. AP-1 transcriptional coactivator redox factor (Ref)-1 was present in the lens epithelium and was association with the AP-1-binding complex during oxidative stress. In the reporter gene assay, only the fragments of the hTTase 5' region, which contained the AP-1-binding site, could activate the CAT reporter gene's expression in an oxidative stress-dependent manner. The mutant with a replaced AP-1-binding site failed to stimulate CAT expression in an oxidation-sensitive manner. The results showed that the c-Jun component in the AP-1-binding complex was transiently phosphorylated during H2O2 treatment. The c-Jun N-terminal kinase or SAPK/JNK, which responds to stress signaling and is the upstream protein kinase of c-Jun, was activated and translocated from cytosol to nucleus under the same conditions. CONCLUSIONS: The data demonstrate that the activation of the hTTase gene under oxidative stress depends on the AP-1 transcription factor. The event was initiated only through an intact cell, possibly mediated through signal transduction by a phosphorylation-dephosphorylation mechanism. As far as the authors know, this is the first evidence of the association of AP-1 with the regulation of hTTase gene expression.

Blotting, Western↗
PubMed2003

Inhibition of the yeast cytochrome bc1 complex by ilicicolin H, a novel inhibitor that acts at the Qn site of the bc1 complex.

Ilicicolin H is an antibiotic isolated from the "imperfect" fungus Cylindrocladium iliciola strain MFC-870. Ilicicolin inhibits mitochondrial respiration by inhibiting the cytochrome bc(1) complex. In order to identify the site of ilicicolin action within the bc(1) complex we have characterized the effects of ilicicolin on the cytochrome bc(1) complex of Saccharomyces cerevisiae. Ilicicolin inhibits ubiquinol-cytochrome c reductase activity of the yeast bc(1) complex with an IC(50) of 3-5 nM, while 200-250 nM ilicicolin was required to obtain comparable inhibition of the bovine bc(1) complex. Ilicicolin blocks oxidation-reduction of cytochrome b through center N of the bc(1) complex and promotes oxidant-induced reduction of cytochrome b but has no effect on oxidation of ubiquinol through center P. These results indicate that ilicicolin binds to the Qn site of the bc(1) complex. Ilicicolin induces a blue shift in the absorption spectrum of ferro-cytochrome b, and titration of the spectral shift indicates binding of one inhibitor molecule per Qn site. The effects of ilicicolin on electron transfer reactions in the bc(1) complex are similar to those of antimycin, another inhibitor that binds to the Qn site of the bc(1) complex. However, because the two inhibitors have different effects on the absorption spectrum of cytochrome b, they differ in their mode of binding to the Qn site.

Antimycin A↗
PubMedDate not supplied

Arsenic in glacial aquifers: sources and geochemical controls.

A total of 176 wells in sand-and-gravel glacial aquifers in central Illinois were sampled for arsenic (As) and other chemical parameters. The results were combined with archived and published data from several hundred well samples to determine potential sources of As and the potential geochemical controls on its solubility and mobility. There was considerable spatial variability in the As concentrations. High concentrations were confined to areas smaller than 1 km in diameter. Arsenic and well depth were uncorrelated. Arsenic solubility appeared to be controlled by oxidation-reduction (redox) conditions, especially the presence of organic matter. Geochemical conditions in the aquifers are typically reducing, but only in the most reducing water does As accumulate in solution. In wells in which total organic carbon (TOC) was below 2 mg/L and sulfate (SO4(2-)) was present, As concentrations were low or below the detection limit (0.5 microg/L). Arsenic concentrations >10 microg/L were almost always found in wells where TOC was >2 mg/L and SO4(2-) was absent or at low concentrations, indicating post-SO4 (2-)reducing conditions. Iron (Fe) is common in the aquifer sediments, and Fe oxide reduction appears to be occurring throughout the aquifers. Arsenic is likely released from the solid phase as Fe oxide is reduced.

Arsenic↗
PubMed2001

Stent coating with titanium-nitride-oxide for reduction of neointimal hyperplasia.

BACKGROUND: Coronary stents prevent constrictive arterial remodeling but stimulate neointimal hyperplasia. Stainless steel induces a metallic foreign body reaction, which is absent for titanium. The hypothesis of the present study was that titanium renders the stent surface biologically inert, with reduced platelet and fibrinogen binding. METHODS AND RESULTS: Twelve pigs were instrumented with a stainless steel and 2 titanium-nitride-oxide-coated stents (TiNOX 1, ceramic; TiNOX 2, metallic). Animals were restudied after 6 weeks. Histological specimens of stented segments were analyzed by digital morphometry. Platelet adhesion and fibrinogen binding studies were performed in the perfusion chamber. Under in vitro conditions, TiNOX 1 showed reduced platelet adhesion (65+/-3%) compared with TiNOX 2 (72+/-5%; P<0.05) and stainless steel (71+/-4%; P<0.05). Platelet adhesion 48 hours after incubation with human plasma, however, was not different between TiNOX 1 (17+/-3%) and 2 (15+/-3%) but was significantly higher with stainless steel (23+/-2%; P<0.05). Fibrinogen binding was significantly reduced with TiNOX 2 (54+/-3%) compared with TiNOX 1 (82+/-4%, P<0.05) or stainless steel (100%, P<0.05). Histomorphometry revealed a significantly larger neointimal area in stainless steel (2.61+/-1.12 mm(2)) than in TiNOX 1-coated (1.47+/-0.84 mm(2), P<0.02) or TiNOX 2-coated (1.39+/-0.93 mm(2), P<0.02) stents. The reductions were 44% and 47%, respectively. CONCLUSIONS: TiNOX coating significantly reduces neointimal hyperplasia in stainless steel stents. The antiproliferative effect was similar for both TiNOX coatings, suggesting that the electrochemical properties are more important for attenuation of neointimal proliferation than the observed differences in platelet adhesion and fibrinogen binding.

Alloys↗
PubMed1989

Anaerobic Carbon Metabolism by the Tricarboxylic Acid Cycle : Evidence for Partial Oxidative and Reductive Pathways during Dark Ammonium Assimilation.

Nitrogen-limited cells of Selenastrum minutum (Naeg.) Collins are able to assimilate NH(4) (+) in the dark under anaerobic conditions. Addition of NH(4) (+) to anaerobic cells results in a threefold increase in tricarboxylic acid cycle (TCAC) CO(2) efflux and an eightfold increase in the rate of anaplerotic carbon fixation via phosphoenolpyruvate carboxylase. Both of these observations are consistent with increased TCAC carbon flow to supply intermediates for amino acid biosynthesis. Addition of H(14)CO(3) (-) to anaerobic cells assimilating NH(4) (+) results in the incorporation of radiolabel into the alpha-carboxyl carbon of glutamic acid. Incorporation of radiolabel into glutamic acid is not simply a short-term phenomenon following NH(4) (+) addition as the specific activity of glutamic acid increases over time. This indicates that this alga is able to maintain partial oxidative TCAC carbon flow while under anoxia to supply alpha-ketoglutarate for glutamate production. During dark aerobic NH(4) (+) assimilation, no radiolabel appears in fumarate or succinate and only a small amount occurs in malate. During anaerobic NH(4) (+) assimilation, these metabolites contain a large proportion of the total radiolabel and radiolabel accumulates in succinate over time. Also, the ratio of dark carbon fixation to NH(4) (+) assimilation is much higher under anaerobic than aerobic conditions. These observations suggest the operation of a partial reductive TCAC from oxaloacetic acid to malate, fumarate, and succinate. Such a pathway might contribute to redox balance in an anaerobic cell maintaining partial oxidative TCAC activity.

Journal Article↗
PubMed1978

Evaluation of oxidative phosphorylation in hearts from euthyroid, hypothyroid, and hyperthyroid rats.

The energy relationships between cytosolic and mitochondrial metabolism were studied in the hearts from euthyroid, hypothyroid, and hyperthyroid rats. Isolated mitochondria showed high respiratory control ratios and impermeability to exogenous NADH. Hypo- and hyperthyroidism, respectively, resulted in lower and higher contents of both cytochromes per mitochondrion and mitochondrial protein per gram of wet weight of heart without changes in the ratio of cytochrome c to cytochrome aa3. In isolated perfused heart, the hyperthyroid state led to an increase in work rate and thereby an elevation of Vo2, which resulted in an increase oxidation-reduction turnover number for the cytochromes. An agreement was found between [ATP]/[ADP][Pi] of cytosolic free adenine nucleotides and the value calculated from a mathematical model of mitochondrial respiration. This implies that mitochondrial respiration is controlled at the cytochrome oxidase reaction and that oxidative phosphorylation in intact tissue is tightly coupled irrespective of thyroid state. It is concluded that thyroid hormone causes an increase in the mitochondrial mass, mitochondrial cytochrome content, and respiratory rate, and consequently expands the capacity of oxidative metabolism without an uncoupling effect on oxidative phosphorylation.

Adenine Nucleotides↗
PubMed2001

Antioxidant and redox regulation of cellular signaling: introduction.

Oxidation-reduction (redox) based regulation of gene expression appears to be a fundamental regulatory mechanism in cell biology. This basic information has been exploited to develop novel strategies in clinical therapeutics. In contrast to the conventional idea that reactive species mostly serve as a trigger for oxidative damage of biological structures, we now know that low physiologically relevant concentration of reactive oxygen species can regulate a variety of key molecular mechanisms. Physical exercise causes redox changes in various cells and tissues. The molecular implications of such change are yet uncharacterized. The five component articles of this symposium discuss skeletal muscle contraction, cell adhesion, heat shock proteins, programmed cell death, and carbohydrate metabolism as they relate to physical exercise.

Antioxidants↗
PubMed1981

Physiological behaviour of Escherichia coli grown in opposing gradients of oxidant and reductant in the gradostat.

Gradients of nutrients are extremely common in nature, and this paper describes changes in the physiology of Escherichia coli grown in the gradostat, a series of five linked vessels with opposing gradients of glucose and of oxygen plus nitrate. Most growth occurred at the aerobic and anaerobic ends of the system. High rates of respiration, high energy charge and high activities of various oxidative enzymes were seen in the two most aerobic vessels; however, oxygen provision was presumably poor, because nitrate reductase activities were also high in this region. Vessels 3 and 4 showed the lowest values for respiration rate, enzyme activity and energy charge, and cells here were both nutrient starved and possibly inhibited by nitrite. Vessel 5 was highly anaerobic, resulting in the presence of hydrogenase activity. It was concluded that cells found in different regions of the gradostat had undergone biochemical differentiation in spatial gradients of electron donors and acceptors.

Adenine Nucleotides↗
PubMed1995

EPR study of the sea anemone cytolysin, equinatoxin II, cytotoxicity on V-79 cells.

Electron paramagnetic resonance (EPR) was used to study the effect of equinatoxin II (EqT II), a cytolytic protein isolated from the sea anemone Actinia equina L., on membrane fluidity and cell metabolism of V-79 cells; the reduction of the spin probe incorporated into the cell membranes as well as the oxygen consumption in the cell suspension were measured. The results were compared with the results obtained by the cell viability study. Under the influence of EqT II (less than 37.5 micrograms/10(6) cells) no significant changes in cell membrane fluidity were observed, while reduction kinetics of the spin probe and the oxygen consumption decreased when the cells were kept in Tris buffer solution. However, in the presence of 10% fetal calf serum, which prevented cell lysis, the effects of EqT II were diminished. The oxygen consumption corresponds to the cell viability changes but the reduction kinetics alterations indicate that some oxidation-reduction processes other than cell respiration are affected by EqT II in the absence of serum. The effect seems to be indirect, probably due to the formation of pores which are associated with changed permeability of plasmalemma for metabolites and ions.

Animals↗
PubMed2003

Oxidative stress and gene expression in sepsis.

Dysregulation of the immuno-inflammatory response, as seen in sepsis, may culminate in host cell and organ damage. Lipopolysaccharide from Gram-negative bacterial cell walls induces gene activation and subsequent inflammatory mediator expression. Gene activation is regulated by a number of transcription factors at the nuclear level, of which nuclear factor kappaB appears to have a central role. The redox (reduction-oxidation) cellular balance is important for normal cellular function, including transcription factor regulation. In sepsis, a state of severe oxidative stress is encountered, with host endogenous antioxidant defences overcome. This has implications for cellular function and the regulation of gene expression. This review gives an overview of the mechanisms by which transcription factor activation and inflammatory mediator overexpression occur in sepsis, together with the events surrounding the state of oxidative stress encountered and the effects on the host's antioxidant defences. The effect of oxidative stress on transcription factor regulation is considered, together with the role of antioxidant repletion in transcription factor activation and in sepsis in general. Other interventions that may modulate transcription factor activation are also highlighted.

Animals↗
PubMed1983

Inhibition of mitochondrial oxidative metabolism by SKF-525A in intact cells and isolated mitochondria.

We have examined the effects of various concentrations of SKF-525A (beta-diethylaminoethyldiphenylpropyl acetate X HCl) on the energy metabolism of liver slices, isolated liver mitochondria, and two types of ascites tumor cells, as well as on ion transport in liver slices. In liver slices, 0.2 to 1.0 mM SKF-525A caused an initial stimulation of O2 uptake which was followed, at 0.5 to 1.0 mM, by a progressive inhibition of O2 consumption, a fall of slice ATP content, and a reduced transport of K+, Na+ and Ca2+. In isolated mitochondria, we studied the effects of SKF-525A on the rate of respiration and on the oxidation-reduction responses of NAD(P)+ and cytochrome b in the presence of various substrates. The results suggest that SKF-525A had three distinct actions on liver mitochondria, viz. an uncoupling action at low concentrations (0.02 to 0.17 mM); at higher concentrations (0.2 to 0.5 mM) an inhibition of the oxidation of NAD(P)+-linked substrates, exerted close to the substrate level; also at 0.2 to 0.5 mM, a less effective inhibition of electron transfer at a point between cytochrome b and O2 in the electron-transfer chain. Experiments on O2 consumption and cytochrome b oxidation-reduction changes in ascites cells showed only the first two of these effects in the intact tumor cells. We conclude that inhibition of mitochondrial energy-conserving reactions by SKF-525A can have a marked influence on energy-requiring aspects of liver-cell metabolism, one example of which is inhibition of cation active transport.

Adenosine Triphosphate↗
PubMed2004

L-gamma-Glutamyl-L-cysteinyl-glycine (glutathione; GSH) and GSH-related enzymes in the regulation of pro- and anti-inflammatory cytokines: a signaling transcriptional scenario for redox(y) immunologic sensor(s)?

Of the antioxidant/prooxidant mechanisms mediating the regulation of inflammatory mediators, particularly cytokines, oxidative stress-related pathways remain a cornerstone. It is conspicuous that there is a strong association between free radical accumulation (ROS/RNS; oxidative stress) and the evolution of inflammation and inflammatory-related responses. The scenario that upholds a consensus on the aforementioned is still evolving to unravel, from an immunologic perspective, the molecular mechanisms associated with ROS/RNS-dependent inflammation. Cytokines are keynote players when it comes to defining an intimate relationship among reduction-oxidation (redox) signals, oxidative stress and inflammation. How close we are to identifying the molecular basis of this intricate association should be weighed against the involvement of specific signaling molecules and, potentially, transcription factors. L-gamma-Glutamyl-L-cysteinyl-glycine, or glutathione (GSH), an antioxidant thiol, has shaped, and still is refining, the face of oxidative signaling in terms of regulating the milieu of inflammatory mediators, ostensibly via the modulation (expression/repression) of oxygen- and redox-responsive transcription factors, hence termed redox(y)-sensitive cofactors. When it comes to the arena of oxygen sensing, oxidative stress and inflammation, nuclear factor-kappaB (NF-kappaB) and hypoxia-inducible factor-1alpha (HIF-1alpha) are key players that determine antioxidant/prooxidant responses with oxidative challenge. It is the theme therein to underlie current understanding of the molecular association hanging between oxidative stress and the evolution of inflammation, walked through an elaborate discussion on the role of transcription factors and cofactors. Would that classify glutathione and other redox signaling cofactors as potential anti-inflammatory molecules emphatically remains of particular interest, especially in the light of identifying upstream and downstream molecular pathways for conceiving therapeutic, alleviating strategy for oxidant-mediated, inflammatory-related disease conditions.

Animals↗
PubMed2006

Simultaneous microbial reduction of iron(III) and arsenic(V) in suspensions of hydrous ferric oxide.

Bacterial reduction of arsenic(V) and iron(III) oxides influences the redox cycling and partitioning of arsenic (As) between solid and aqueous phases in sediment-porewater systems. Two types of anaerobic bacterial incubations were designed to probe the relative order of As(V) and Fe(III) oxide reduction and to measure the effect of adsorbed As species on the rate of iron reduction, using hydrous ferric oxide (HFO) as the iron substrate. In one set of experiments, HFO was pre-equilibrated with As(V) and inoculated with fresh sediment from Haiwee Reservoir (Olancha, CA), an As-impacted field site. The second set of incubations consisted of HFO (without As) and As(III)- and As(V)- equilibrated HFO incubated with Shewanella sp. ANA-3 wild-type (WT) and ANA-3deltaarrA, a mutant unable to produce the respiratory As(V) reductase. Of the two pathways for microbial As(V) reduction (respiration and detoxification), the respiratory pathway was dominant under these experimental conditions. In addition, As(III) adsorbed onto the surface of HFO enhanced the rate of microbial Fe(III) reduction. In the sediment and ANA-3 incubations, As(V) was reduced simultaneously or prior to Fe(III), consistent with thermodynamic calculations based on the chemical conditions of the ANA-3 WT incubations.

Acetates↗
PubMed1975

The effect of trimethadione on brain energy metabolism and EEG activity of the conscious rat exposed to HPO.

The use of trimethadione (TMO) as a protector in hyperbaric oxygen toxicity in the conscious rat has been examined in detail. The oxidation-reduction state of pyridine nucleotides was measured simultaneously with the EEG activity from the surface of the brain cortex. From the data obtained, a few parameters were calculated. The results show that in TMO-treated animals the time to the onset of convulsions, the time to the onset of NADH oxidation-reduction cycles, and the survival time were significantly longer than in the control group. The effect of TMO on the EEG shows that the tonic phase of the convulsive activity was almost completely abolished.

Animals↗
PubMed1981

[Effect of antibiotics and stimulants on the functional activity of cultured macrophages].

Kanamycin and ampicillin alone or in combination with leucocytic pyrogen, pyrogenal and prodigiozan were tested in cultures of peritoneal macrophages infected with Shigella. The function of the cells was estimated by the phagocytosis indices (with an account of the phases of the Shigella absorption and digestion) and activity of the oxidation-reduction (the NBT test) and hydrolytic (acid phosphatase) enzymes. The inhibitory effect of the antibiotics on the functional activity of the cultivated macrophages was shown. In the presence of kanamycin a decrease in the absorptive and digestive functions of the cells with respect to Shigella was observed. The decreased activity of the oxidation-reduction enzymes and acid phosphatase in the cells almost at all observation periods was also evident of inhibition of the phagocytosis terminal phase, i.e. the intracellular digestion of the bacteria. The use of ampicillin resulted in lower levels of Shigella absorption, while the phase of the bacteria digestion remained pronounced. At the same time the decreased activity of the lysosomal enzyme (acid phosphatase) participating in intracellular digestion of Shigella was characteristic of a clear tendency to their inhibition in the presence of ampicillin. The preliminary treatment of the cells with leucocytic pyrogen, pyrogenal and prodigiozan eliminated partially or completely the inhibitory effect of the antibiotics on the functional activity of the cultivated macrophages.

Ampicillin↗