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At least 919 records · Page 51Linked to original sources

PubMed1977

Absence of autoregulation in peripheral nerve blood flow.

Blood flow was measured in the sciatic nerve of cats utilizing the method of hydrogen polarography. The mean baseline blood flow for all animals was found to be 47.1 ml/100 g/min +/- 14.9 SD. The flow changes produced by lowering the blood pressure by exsanguination and elevation by the use of angiotensin were then evaluated. The highest (normal) levels of blood flow were observed between the mean blood pressures of 80-110 mm Hg. At mean systemic arterial pressures of less than 85, there was a marked decrease in peripheral nerve blood flow with no detectable flow being measured below mean systemic pressures of 50 mm Hg. Above 105 mm Hg mean arterial pressure, there was a very gradual and progressive decline in blood flow to the levels measured at 200 mm Hg. These findings indicate a complete absence of vascular autoregulation in the peripheral nerve trunks.

Animals↗

PubMed1994

A 31P magnetic resonance spectroscopy study of mitochondrial function in skeletal muscle of patients with Parkinson's disease.

The activity of complex I of the respiratory chain is decreased in the substantia nigra of patients with Parkinson's disease (PD) but the presence of this defect in skeletal muscle is controversial. Therefore, the mitochondrial function of skeletal muscle in patients with PD was investigated in vivo using 31P magnetic resonance spectroscopy. Results from 7 PD patients, 11 age matched controls and 9 mitochondrial myopathy patients with proven complex I deficiency were obtained from finger flexor muscle at rest, during exercise and in recovery from exercise. In resting muscle, the patients with mitochondrial myopathy showed a low PCr/ATP ratio, a low phosphorylation potential, a high P(i)/PCr ratio and a high calculated free [ADP]. During exercise, stores of high energy phosphate were depleted more rapidly than normal, while in recovery, the concentration of phosphocreatine and free ADP returned to pre-exercise values more slowly than normal. In contrast, the patients with PD were not significantly different from normal for any of these variables, and no abnormality of muscle energetics was detected. Three of the PD patients also had mitochondrial function assessed biochemically in muscle biopsies. No respiratory chain defect was identified in any of these patients by polarography or enzyme analysis when compared with age-matched controls. These results suggest that skeletal muscle is not a suitable tissue for the investigation and identification of the biochemical basis of the nigral complex I deficiency in PD.

Adolescent↗

PubMed1995

Effects of acetyl- and proprionyl-L-carnitine on peripheral nerve function and vascular supply in experimental diabetes.

L-Carnitine metabolism is abnormal in diabetes mellitus, and treatment with acetyl-L-carnitine (ALC) improves the function of cardiac muscle, retina, and peripheral nerve in experimental models. The aim was to compare the effects of ALC and proprionyl-L-carnitine (PLC) on motor and sensory nerve conduction in streptozotocin-diabetic rats and to ascertain whether their action could be mediated by a vascular mechanism. ALC and PLC treatment for 2 months after diabetes induction attenuated the development of sciatic motor nerve conduction velocity (NCV) deficits by 59.4% +/- 4.4% and 46.9% +/- 3.2%, respectively. There was a similar level of protection for sensory saphenous NCV (42.9% +/- 6.6% and 47.8% +/- 6.0%, respectively). Neither ALC nor PLC prevented the development of resistance to hypoxic conduction failure (RHCF) in sciatic nerve from diabetic rats. A 46.5% +/- 3.4% deficit in sciatic endoneurial blood flow, measured by microelectrode polarography and hydrogen clearance, in diabetic rats was partially prevented by both ALC (48.7% +/- 6.4%) and PLC (69.4% +/- 10.1%). ALC had no significant effect on blood flow in nondiabetic rats. Thus, the data show that these L-carnitine derivatives have a similar efficacy in preventing nerve dysfunction, which depends on a neurovascular action.

Acetylcarnitine↗

PubMed1987

Metal ion binding by biological surfaces: voltammetric assessment in the presence of bacteria.

Voltammetric techniques (differential pulse polarography (DPP) and differential pulse anodic stripping voltammetry (DPASV)) were evaluated for their capability to distinguish, without prior separation of the solid phase (e.g. filtration, centrifugation), between dissolved and particulate concentrations of Zn(II), Pb(II) and Cu(II), and to measure the extent of binding of these metals to the surface of a bacterium (Klebsiella pneumonia, formaldehyde treated). From titration curves of bacterial cell suspensions with metals the specific adsorption of metals was determined and quantified in terms of average surface complex formation constants and differential equilibrium functions. The following stability sequence for surface complexes was found: Cu2+ greater than Pb2+ greater than Zn2+ much greater than Ca2+. Simultaneous analytical determination permitted the measurement of both the binding of Cu(II) to the cell surface, and the binding to the solute exudate ligands. The affinity of the metal ions for the functional groups of the cell surface is strongly pH-dependent, and, at a given pH, decreases with increasing metal loading of the bacterial surfaces. This indicates that metal ions bind first to the highest affinity surface ligands and subsequently to those of lesser activity. Copper(II) appears to form stronger surface complexes with the high affinity ligands of the bacterial surface than with the functional groups of hydrous oxides.

Cell Membrane↗

PubMed1984

Interaction of alpha-thrombin and prethrombin 2, with phosphatidylserine-containing monolayers.

Prothrombin activation complex is located at a phospholipid surface on activated platelets. To see whether the thrombin domain of the molecule plays a role in the interaction with lipids, we investigated the direct interaction of human alpha-thrombin and its precursor prethrombin 2 with phospholipid monolayers of various compositions (PS/PC). Adsorption of the labeled proteins was determined by surface radioactivity measurements. Penetration of the proteins in the lipid layer was inferred from capacitance variation of the monolayer, measured by a.c. polarography. Disulfide bridges reduced at the electrode were determined by cyclic voltametry. In all the cases studied, although in different manners thrombin was found both to adsorb and penetrate the lipid layer, whereas prethrombin 2 did not penetrate pure phosphatidylcholine (PC). In the case of thrombin, but not of prethrombin 2, penetration is accompanied by S-S reduction which is maximum at 10 per cent of phosphatidylserine (PS). This indicates a different orientation for prethrombin 2 and thrombin in the lipid layer. This observation might be of importance for the comprehension of the architecture of the prothrombin activation complex and for the regulation of thrombin formation within the complex.

Enzyme Activation↗

PubMed1989

Interaction of human gamma-carboxyglutamic acid domainless prothrombin with phospholipids.

The conversion of prothrombin into thrombin occurs at the surface of stimulated platelets. In order to see the influence of gamma-carboxyglutamic acid in the interaction of prothrombin with phospholipid, we investigated the direct interaction of the peptide 1-41 and prothrombin (des 1-44) with phospholipid monolayers of various compositions. Adsorption of the labeled proteins was determined by surface radioactivity measurements. Penetration of the proteins into the lipid layers was inferred from capacitance variation of the monolayer, measured by a.c. polarography. Prothrombin (des 1-44) was found both to adsorb and to penetrate the lipid monolayers, in the presence and in the absence of Ca++. The effects are higher on 100% PS than on 25% PS. This protein was also found to increase the permeability of vesicles containing 25% PS to T1+ ions, in the presence and in the absence of Ca++. Comparison with prothrombin shows that Gla residues are clearly involved in the interaction at 25% PS; nevertheless, the peptide 1-41 does not penetrate. A model of interaction of prothrombin with phospholipid, including both adsorption of prothrombin by Gla residues and its penetration by another domain, is proposed.

1-Carboxyglutamic Acid↗

PubMed1985

Electrochemical and electron spin resonance studies of actinomycin D and other phenoxazones.

Electrochemical studies on actinomycin D (1) and two analogs, 2-amino-3-phenoxazone (2) and 1,2,4-trichloro-7-nitrophenoxazone (3) were analyzed by polarography and ESR spectroscopy. The polarograms of the three compounds in acetonitrile all show two reduction waves. ESR experiments confirm that the first reduction wave corresponds to a one-electron transfer process which produces a phenoxazone free radical anion and the second wave corresponds to a subsequent one-electron transfer producing a diamagnetic dianion. Substitution with electron-withdrawing groups such as NO2 (at C-7) and chloro (at C-1, C-2 and C-4)3 facilitated the reduction of the phenoxazone ring system to a free radical (i.e., half-wave potentials; 1, -0.815 V; 2, -0.920 V; 3, -0.135 V). It was found, by computer simulation of the ESR spectra, that the spin density in the electrochemically generated free radicals from 1, 2 and 3 was preferentially located in the benzenoid ring and at the N-10 nitrogen. For radicals obtained from 1 and 2, only a small residual spin density could be detected in the quinoid ring. Since 1 can be metabolized to a free radical in cells, these free radical forms of 1 and its analogs may represent reactive forms of the phenoxazone nucleus.

Anions↗

PubMed1991

Biophysical studies of the complexes of polyriboguanylic acid with brominated and chlorinated polyribocytidylic acids.

Conformation of double-stranded complexes of polyriboguanylic acid with halogenated polyribocytidylic acid [poly(C)] was studied with the aid of differential pulse polarography, terbium fluorescence and circular dichroism spectrometry. It was shown that halogenation at C(5) of cytosine residues in poly(C) disturbed the ordered structure of the double-helical complex. In addition, this halogenation does not improve antiviral activity of the polynucleotide complex studied in the system of vesicular stomatitis virus and the cell culture of chicken embryos. It was concluded that the regularity of the secondary structure of synthetic RNAs might play an important role in the mechanism of biological activity of these biomacromolecules.

Biophysical Phenomena↗

PubMed1984

An improved differential pulse voltammetry technique allows the simultaneous analysis of dopaminergic and serotonergic activities in vivo with a single carbon-fibre electrode.

Differential pulse voltammetry has successfully been employed to study either 5-hydroxyindoles, or ascorbic acid and catechols in the brain of anaesthetised or freely moving rats. A new electrochemical pretreatment of pyrolytic carbon-fibre electrodes has been developed, enabling the simultaneous recording of all three compounds in the striatum of anaesthetised rats, using a Tacussel polarography. Furthermore, a fourth peak was recorded at +450 mV. Pharmacological treatments performed to define the nature of the four peaks recorded in the striatum confirmed that peak 1 corresponds to ascorbic acid, peak 2 to dihydroxyphenylacetic acid, peak 3 to 5-hydroxyindoleacetic acid and peak 4 to homovanillic acid.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1987

Inhibition of ATP synthesis by 1-methyl-4-phenylpyridinium ion (MPP+) in isolated mitochondria from mouse brains.

Effect of 1-methyl-4-phenylpyridinium ion (MPP+) on adenosine triphosphate (ATP) synthesis was studied using isolated mitochondrial preparations from mouse brains. Oxidation of glutamate + malate in the mitochondria estimated by polarography was significantly inhibited by MPP+, and synthesis of ATP was inhibited to approximately 9% of that of control by 0.06 mM of MPP+. Oxidation of alpha-glycerophosphate and succinate was not inhibited, and ATP was synthesized normally. Energy crisis appears to be one of the most important mechanisms of neuronal degeneration in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced experimental parkinsonism.

1-Methyl-4-phenylpyridinium↗

PubMed1986

Oxygen and nitroreductase-dependent binding of AF-2 in spheroids and murine tumors.

Fluorescent nitroheterocycles such as AF-2 may be useful in identifying hypoxic cells in tumors. Since binding is dependent on rate of drug metabolism (nitroreduction) as well as cellular oxygen content, flow cytometric analysis of cells from tumors and spheroids was used to quantify AF-2 binding, and differential pulse polarography was used to measure reduction of AF-2 by several mammalian cell lines, spheroids and tumor cells. Hypoxic V79 spheroid cells and Lewis lung tumor cells bound 20 times more AF-2 than oxic cells, and binding proceeded with first order kinetics. Nitroreductase activity varied about tenfold among different tumor cells. As expected, the rate of binding of AF-2 correlated well with the rate of nitroreduction. Oral injection of AF-2 (5 mg) was the most successful method of administration to tumor-bearing mice. In mice injected with both AF-2 and Hoechst 33342 (which stains well-perfused cells), SCCVII tumor cells which contained the most Hoechst contained the least AF-2. Although minimal toxicity by AF-2 was observed in these tumors, binding of AF-2 was barely sufficient for detection using flow cytometry.

Animals↗

PubMed1983

Hepatic metallothionein and resistance to copper in juvenile coho salmon.

1. Four groups of 600 juvenile coho salmon (Oncorhynchus kisutch) of 3-8g body weight were exposed to sublethal concentrations of copper acetate in water of hardness 280 mg/l (as CaCO3). 2. Flow-through conditions were maintained for a period of 10 weeks, during which the copper concentrations to which the groups of fish were exposed were approximately 1, 50, 100 and 150 micrograms Cu/l. 3. Hepatic metallothionein concentrations were measured using differential pulse polarography in filtrates of heat-denatured saline extracts of the tissues. 4. These values increased as a function of the copper concentration to maximum levels after 4 weeks of continuous exposure and thereafter remained more or less constant. 5. Flow-through 168 hr LC50 values for fish tested at intervals throughout the experiment increased to maximum values (2.5 X control values) at 1 week and during the next 3 weeks fell somewhat to stable but elevated values. 6. At 4 weeks, these were related to the metallothionein (MT) values by the regression equation 168 hr LC50 = 2.423 (+/- 0.455) X MT + 48.6 (+/- 31.1). 7. The probability that the relationship was not accidental exceeded 97%.

Animals↗

PubMed1994

Influence of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors on mitochondrial respiration in rat liver during ischemia.

Effects of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, pravastatin and simvastatin, on mitochondrial respiration in ischemic rat liver were examined. Either vehicle, pravastatin (2 or 4 mg/kg per day), or simvastatin (1 or 2 mg/kg per day) was orally administered for 3 weeks. Liver ischemia was induced by cessation of the systemic circulation for 60 min. Liver mitochondria were isolated and the respiration was determined by polarography using glutamate and succinate as substrates. In the vehicle-treated group, ischemia drcreased ZO3, respiratory control index (RCI: QO3/QO4), and ADP/O ratio. Pretreatments with pravastatin and simvastatin enhanced the decreases in QO3 measured with either glutamate or succinate, and in ADP/O ratio measured with succinate. Because of decreasing QO4, HMG-CoA reductase inhibitors did not modify the changes in RCI due to ischemia. There were no significant differences in respiratory indices between pravastatin- and simvastatin-treated groups. In conclusion, HMG-CoA reductase inhibitors may enhance respiratory impairment of liver mitochondria under pathophysiological conditions, such as ischemia.

Adenosine Diphosphate↗

PubMed1995

Effects of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors on mitochondrial respiration in ischemic rat hearts.

The aim of the present study was to examine the effects of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors on mitochondrial respiration in ischemic rat hearts, and to compare the effects between water-soluble pravastatin and lipid-soluble simvastatin. Either vehicle (0.5% carboxymethyl cellulose), pravastatin (2 or 4 mg/kg per day), or simvastatin (1 or 2 mg/kg per day) was orally administered for 3 weeks. Ischemia was induced by ligating the aorta for 60 min in anesthetized open chest rats under artificial respiration. The hearts were removed, mitochondria were isolated, and the respiration was determined by polarography using glutamate and succinate as substrates. When succinate was used as a substrate, the ADP-stimulated respiration (QO3) and ATP production per unit oxygen (ADP/O ratio) were decreased by ischemia. The decreases in QO3 and ADP/O ratio in the pravastatin- and simvastatin-treated groups appeared to be more prominent than those in the vehicle-treated group. This was especially true in the simvastatin-treated group. The ADP-limited respiration (QO4) with succinate in the vehicle-treated heart was slightly increased by ischemia, while that in the pravastatin- or simvastatin-treated hearts was decreased. In conclusion, HMG-CoA reductase inhibitors may result in worsening of myocardial mitochondrial respiration during ischemia.

Adenosine Diphosphate↗

PubMed2005

Cellular biomarkers of exposure and biological effect in hepatocytes of turbot (Scophthalmus maximus) exposed to Cd, Cu and Zn and after depuration.

Cellular biomarkers of exposure and biological effects were measured in hepatocytes of turbot exposed to either Cd, Cu or Zn at concentrations of 1 and 10 mg/l seawater for 7 days and after depuration for 14 days. Metal content in hepatocyte lysosomes was determined by image analysis after autometallography (AMG) as volume density of autometallographed black silver deposits (Vv(BSD)). Metallothionein (MT) levels were quantified on liver sections by microdensitometry after immunohistochemical staining with a polyclonal anti cod-MT antibody (MT-OD), and in the cytosolic fraction of hepatocytes by difference pulse polarography (MT-DPP). Lysosomal structural changes (lysosomal volume, surface and numerical densities--Vv(LYS), Sv(LYS) and Nv(LYS-), and surface-to-volume ratio S/V(Lys)) were quantified by image analysis after demonstration of beta-glucuronidase activity on liver cryotome sections. Vacuolisation produced by metal-exposure in hepatocytes was quantified by stereology as volume density of vacuoles (Vv(VAC)). Exposure time and metal concentrations significantly affected Vv(BSD) in lysosomes, MT levels and the degree of vacuolisation after 1 h and 1 day exposure to the three metals. The highest Vv(BSD), MT and Vv(VAC) values were recorded after 7 days exposure in all cases. MT-OD and MT-DPP were significantly correlated with Vv(BSD). Vv(LYS) in hepatocytes increased significantly after exposure to the metals. Exposure biomarkers returned to control values after depuration with the exception of those turbots that had been exposed to 10 mg Cd/l. Alike, Vv(LYS) and Sv(lys) (Cu exposure) and Nv(LYS) (Cd and Zn exposures) returned to control values after depuration. It has been therefore demonstrated that the biomarkers used are reversible and return towards control levels once metal exposure ceases. Overall, it is concluded that Vv(BSD), MT-levels and lysosomal responses are valuable biomarkers to assess metal exposure and its effects in turbot, although in quantitative terms the biomarker response varied between metals.

Analysis of Variance↗

PubMed2005

Interaction of an amphitropic protein (factor Xa) with membrane models in a complex system.

Phosphatidylserine (PS) plays a crucial role, in the conversion of prothrombin into thrombin by the protease, factor Xa. Physiologically, the conversion occurs in the prothrombinase complex. The question of how water-soluble proteins that normally circulate in plasma bind remains to be unambiguously determined. We previously found that the amphitropic proteins (prothrombin, factors V and Va) penetrate into phospholipid layers. AC polarography has allowed the detection for the first time of insertion of factor Xa into condensed monolayers containing phosphatidylserine (PS) and phosphatidylcholine (PC) either 100% PS or 25% PS in the presence of Ca2+. This observation demonstrates that part of factor Xa can cross the phospholipid polar headgroup/hydrocarbon chain interface. In parallel experiments, radioactive surface measurements permitted measuring binding of tritium-labeled factor Xa onto a PS monolayer and calculate an association constant, 6x10(6) M(-1). Penetration of factor Xa into PS-containing vesicles was investigated also using photoactivable 5-[125I]iodonaphthalene-1-azide, which binds selectively to the lipid embedded domains of the protein. These experiments suggest that Factor Xa penetrates preferentially by its heavy chain, an alternative mode of binding to the commonly accepted binding via its Gla domain. Interaction of factor Xa with PS vesicles also changes its apparent K(m) for S 2222.

Animals↗

PubMed2004

Comparative investigation between acetylcholinesterase obtained from commercial sources and genetically modified Drosophila melanogaster: application in amperometric biosensors for methamidophos pesticide detection.

Genetically modified acetylcholinesterase (AChE) from Drosophila melanogaster (dm) and from commercial sources, Electric eel (ee), Bovine erythrocites (be) and Human erythrocites (he), were investigated as biological receptors for the detection of methamidophos pesticide based on inhibition studies. Most engineered variant of AChE from dm showed enhanced sensitivity toward methamidophos pesticide. Among 24 dmAChE variants tested, 12 presented a sensitivity comparable to the commercially available eeAChE, but higher than AChEs from be and he. Four were found more sensitive and six others were insensitive to methamidophos insecticide. The D375G,Y370F,Y374A,F376L mutant was the most sensitive, with a ki value of 2.2 X 10(6) mol(-1) L min(-1), three orders of magnitude higher than eeAChE (1.1 X 10(3) mol(-1) L min(-1)). The sensor constructed with genetically modified enzyme showed better characteristics with respect to detection limit and sensitivity compared with those using commercial eeAChE. Differential pulse polarography and chronoamperometry were used as electrochemical techniques to characterize the AChE biosensors. The lower detection limit of 1 ppb was obtained with D375G,Y370F,Y374A,F376L mutant of dmAChE, compared to 90 ppb for the commercial eeAChE. This study may stimulate scientists to develop more sensitive and selective procedures for organophosphorus insecticides detection by using engineered variant of dmAChE.

Acetylcholinesterase↗

PubMed2004

Cu(II) complex formation with xylitol in alkaline solutions.

The formation of four Cu(II)-xylitol complexes was observed in aqueous alkaline solutions (11.0< or =pH< or =14.0, I=1.0, 20 degrees C) by means of direct current polarography and VIS spectrophotometry. Mononuclear hydroxy complexes, CuXyl(OH)- (log beta=17.7 +/- 0.5), CuXyl(OH)2(2-) (log beta=20.2 +/- 0.3) and CuXyl2(OH)2(4-) (log beta=22.4 +/- 0.3), are formed at high ligand-to-metal ratios (L:M> or =10), whereas dinuclear complex Cu2Xyl (log beta=29.2 +/- 0.3) is the predominant species at low ligand-to-metal ratio (L:M=0.5). Diffusion coefficients and molar absorptivities of the complex species were determined. pH variable 13C NMR suggested that pKa values of xylitol are rather similar and equal to 13.8 +/- 0.2, 13.9 +/- 0.1 and 13.9 +/- 0.2 for OH-groups adjacent to (C-1,C-5), (C-3) and (C-2,C-4) carbon atoms, respectively.

Alkalies↗