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PubMed1984

Determination of cyanide and thiocyanate in blood plasma and red cells by high-performance liquid chromatography with fluorometric detection.

A method for the determination of cyanide and thiocyanate in blood plasma and red cells of humans was established. It involved high-performance liquid chromatography and fluorometric detection by the König reaction. Calibration curves for cyanide and thiocyanate were linear in the range 1-200 pmol and 2-300 pmol, respectively. Clean-up methods for the determination of cyanide and thiocyanate in red cells were also developed. These methods were applied for the determination of cyanide and thiocyanate in the blood of smokers and non-smokers.

Ascorbic Acid↗
PubMed1990

Displacement chromatography on cyclodextrin-silicas. III. Enantiomer separations.

The feasibility of preparative enantiomer separations by displacement chromatography on analytical-scale beta-cyclodextrin-silica columns, operated in the reversed-phase mode, was demonstrated using the enantiomers of mephobarbital, hexobarbital, dansylleucine, dansylvaline and dansylphenylalanine as model solutes. The method development scheme (which relies on the determination of the elution-mode retention behavior and the adsorption isotherms of the solutes and the candidate displacers) described in Parts I and II can be used to select the appropriate displacers and the conditions leading to a successful displacement chromatographic separation. The importance of the displacer (both type and concentration) to the success of the displacement chromatographic separation is demonstrated.

Amino Acids↗
PubMedDate not supplied

Presence of pro-oxidants in plasma of patients suffering from falciparum malaria.

Haemolysis is the major cause of anaemia in acute Plasmodium falciparum malaria, destroying both parasitized and non-parasitized erythrocytes. Oxidative stress on erythrocytes is considered an important mechanism of haemolysis. Since non-parasitized erythrocytes are also destroyed, the extracellular environment of the erythrocyte may be a contributor to the oxidative stress. To examine the influence of extracellular factors on oxidative stress and haemolysis, baseline values of erythrocyte thio-barbituric acid-reactive substance (ETBAR) and haemolytic indices such as plasma haemoglobin and lactate dehydrogenase (LDH) were estimated in 19 children in Orissa (India) with acute P. falciparum malaria (haemoglobin level < or = 70 g/L). The indices were measured after incubating cross-matched isogroup adult control erythrocytes with patient's plasma, and patient's erythrocytes with adult control plasma both in presence of and in absence of t-butyl hydroperoxide (t-BHP). The procedure was repeated in the blood of 19 age- and sex-matched non-malarial children. Baseline plasma LDH, haemoglobin and ETBAR concentrations were significantly greater in malaria patients than non-malarial children (P < 0.001 for all). Post-incubation values of ETBAR and plasma haemoglobin were significantly higher (P < 0.05) when adult control erythrocytes were incubated with patient plasma, and plasma haemoglobin was significantly higher (P < 0.05) in incubates of patient erythrocytes with adult control plasma, than their respective pre-incubation values when incubated in absence of t-BHP. These differences were not noticed in the incubates of non-malarial children with healthy adult control samples. When incubated in presence of t-BHP all the post-incubation values in the patients were significantly higher than their respective pre-incubation values and post-incubation values without t-BHP (P < 0.001). In non-malarial control samples, only ETBAR concentration was higher than their respective pre-incubation and post-incubation values without t-BHP (P < 0.01). All the values for post-incubation samples with t-BHP were significantly higher in patients than controls (P < 0.001). In post-incubation samples of control erythrocytes and patient plasma in presence of t-BHP, ETBAR correlated inversely with pre-incubation haptoglobin values (P < 0.001). Thus, plasma of acute malaria patients appears to contain pro-oxidants, which may contribute to extracellular oxidative stress on both parasitized and non-parasitized erythrocytes.

Analysis of Variance↗
PubMed2001

Predictors of restenosis after coronary angioplasty. A study on demographic and metabolic variables.

OBJECTIVE: The major concern about percutaneous transluminal coronary angioplasty (PTCA) is the high incidence of restenosis. METHODS: Demographic, clinical and biochemical data were recorded 2 weeks prior to PTCA in 388 patients fulfilling the criteria for initial stenosis, successful PTCA, and angiographic follow-up after 6 months. Restenosis was evaluated by quantitative coronary angiography. RESULTS: Variables predictive of restenosis in univariate analysis were diabetes mellitus, male gender, and the levels of high density lipoprotein (HDL) cholesterol, apolipoprotein A1 (Apo A1) and thio-barbituric acid-reactive substances (TBARS). In trend analysis through quartiles TBARS and fasting glucose levels were significantly associated with restenosis (p = 0.016 and 0.044, respectively), whereas the negative predictivity of Apo A1 and HDL-cholesterol were of borderline significance. In multivariate analysis male gender and diabetes mellitus showed predictivity of significance, and a negative predictivity was also apparent for HDL-cholesterol. CONCLUSION: We conclude that diabetes mellitus, male gender, and low HDL-cholesterol are predictors of restenosis 6 months after PTCA. In addition, TBARS may be a marker for the development of restenosis after PTCA.

Adult↗
PubMed1981

A possible neurochemical basis of the central stimulatory effects of pp'DDT.

The striatal neurochemical changes induced by pp'DDT (600 mg/kg) in mice were: an increase in the concentration of free ammonia, a decrease in the level of GABA and a reduction in the level of acetylcholine. These changes were maximal 5 h after treatment with pp'DDT, when the animals developed 'severe' convulsions. The convulsions and striatal neurochemical changes were modified to different degrees by barbiturates. Phenobarbitone protected all the animals from pp'DDT-induced convulsions. The levels of striatal acetylcholine and GABA in these animals were within normal limits. Prominal reduced the severity of convulsions in pp'DDT-treated animals. The levels of striatal acetylcholine and GABA were significantly lower than control values in these animals. Primidone neither modified the convulsions nor the striatal neurochemical changes in pp'DDT-treated animals. The increase in the concentration of free ammonia, in pp'DDT-treated animals, was not modified by barbiturates. Aminooxyacetic acid raised the GABA level above normal and abolished the convulsions in pp'DDT-treated animals; the level of acetylcholine was within normal limits in these animals. Hydroxylamine produced a similar but less marked effect. Pyridoxine had no effect on convulsions or striatal neurochemical changes induced by pp'DDT. The increase in the concentration of free ammonia in pp'DDT-treated animals was not modified by these agents. It is likely that pp'DDT produced stimulatory effects by increasing the concentration of free ammonia which may be involved in reducing the level of GABA, while changes in the level of acetylcholine may be an effect of pp'DDT-induced convulsions.

Acetylcholine↗
PubMed1995

Volume-activated chloride channels in HL-60 cells: potent inhibition by an oxonol dye.

When swollen in hypotonic media, HL-60 cells exhibit a regulatory volume decrease (RVD) response as a result of net losses of K+ and Cl-. This is primarily caused by a dramatic increase in Cl- permeability, which may reflect the opening of volume-sensitive channels (11). To test this hypothesis, we measured volume-activated Cl- currents in HL-60 cells using the patch-clamp technique. The whole cell Cl- conductance (in nS/pF at 100 mV) increased from 0.09 +/- 0.06 to 1.15 +/- 0.19 to 1.64 +/- 0.40 as the tonicity (in mosmol/kgH2O) of the external medium was decreased from 334 to 263 to 164, respectively. Cl- currents showed no significant inactivation during 800-ms pulses. Current-voltage curves exhibited outward rectification and were identical at holding potentials of 0 or -50 mV, suggesting that the gating of the channels is voltage independent. The selectivity sequence, based on permeability ratios (PX/PCl) calculated from the shifts of the reversal potentials, was SCN- > I- approximately NO3- > Br- > Cl- >> gluconate. 4-Acetamido-4'- isothiocyanostilbene-2,2'-disulfonic acid (SITS; 0.5 mM) inhibits HL-60 Cl- channels in a voltage-dependent manner, with approximately 10-fold increased affinity at potentials greater than +40 mV. Voltage-dependent blockade by SITS indicates that the binding site is located near the outside, where it senses 20% of the membrane potential. These Cl- channels were also inhibited in a voltage-independent manner by the oxonol dye bis-(1,3-dibutylbarbituric acid)pentamethine oxonol [diBA-(5)-C4] with a concentration that gives half inhibition (IC50) of 1.8 microM at room temperature. A similar apparent IC50 value (1.2 microM) was observed for net 36Cl- efflux into a Cl(-)-free hypotonic medium at 21 degrees C. It seems likely, therefore, that the volume-activated Cl- channels are responsible for the net Cl- efflux during RVD. These Cl- channels have properties similar to the "mini-Cl-" channels described in lymphocytes and neutrophils and are strongly inhibited by low concentrations of diBA-(5)-C4.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗
PubMed1983

Brain receptors and zopiclone.

Zopiclone (ZPC; RP 27,267), which is chemically unrelated to benzodiazepines (BZD), was found to have a similar pharmacological profile and to possess in man hypnotic activity similar to that of some BZD such as nitrazepam. It was, therefore, interesting to study the interaction of ZPC with rat brain receptors and specially with the so-called 'BZD receptors'. ZPC possesses in three rat brain regions a high affinity for BZD receptors: its Ki values measured against [3H]-flunitrazepam are 24 nM in the cerebral cortex, 31 nM in the cerebellum, and 36 nM in the hippocampus. No other brain receptors such as gamma-aminobutyric acid receptor, dopamine receptor, serotonin and noradrenergic receptors are reached by ZPC. Moreover, ZPC seems to bind only to brain BZD receptors and, contrarily to some BZD such as flunitrazepam, it does not reach the peripheral renal BZD-binding sites. The synthesis of [3H]-ZPC has permitted a more in-depth study of the interaction of ZPC with brain receptors. The high affinity of ZPC has been confirmed by equilibrium-binding studies (KD = 13 +/- 4 nM in rat hippocampus) and the study of the modulating effect of gamma-aminobutyric acid and barbiturates on ZPC binding has revealed some differences between ZPC and BZD. It could, therefore, be postulated that ZPC might bind in rat brain to sites which do not correspond exactly to BZD sites.

Animals↗
PubMed1975

Enhancement of hepatic microsomal drug metabolism in vitro following ethanol administration.

1. Administration of ethanol intraperitoneally at low dosages (10-25 mg/kg) to rats stimulates hepatic microsomal mixed-function oxidase activity in vitro. 2. Pretreatment with ethanol administered orally has no effect on in vivo drug metabolism as measured by pentobarbitone plasma half-life and has no effect on the excretion of ascorbic acid. Ethanol administration does not enhance its own binding to cytochrome P-450. 3. These observations suggest that the administration of ethanol, at moderate dosage, does not give rise to induction of hepatic cytochrome P-450. 4. Unwashed hepatic microsomes are contaminated with alcohol dehydrogenase, but pretreatment with ethanol does not increase microsomal generation of NADH. 5. Pretreatment with ethanol has no stimulatory effect on NADH-NADP+ transhydrogenation. 6. The stimulation of hepatic drug metabolism in vitro following administration of ethanol is not due to increased cytochrome P-450 nor to increased NADPH, per se, but appears to result from an increase in the activity of NADPH-cytochrome c reductase.

Animals↗
PubMed1989

An iron chelator is not required for reductive iron release from ferritin by radical generating systems.

Although a number of reducing systems can release iron from ferritin, there is debate as to whether the process additionally requires a chelator. We have studied ferritin iron release by microsomes, paraquat and NADPH, by dialuric acid and by hypoxanthine and xanthine oxidase, using ferrozine to complex the released iron. In each case, Fe2+ (ferrozine) formation was detectable when the ferrozine was added at the beginning of the 10 min reaction period, but not at the end. However, with catalase present, up to 0.7 times as much Fe2+ could be measured with ferrozine added at the end. Further Fe2+ could be recovered by adding ascorbate with the ferrozine. These results indicate that an iron chelator is not required for reductive iron release from ferritin. However, the released iron will not be detectable as Fe2+ unless it forms a complex that is resistant to oxidation by H2O2 or other oxidants.

Animals↗
PubMed1999

[Pharmacologic cytoprotection of the central nervous system].

Ischaemia of the central nervous system is considered to be a phenomenon, which manifests after the ischaemic episode and has limited therapeutic possibilities. Clinical situations in which the oxygen supply may be reduced include the following: stroke and transient ischaemic attacks, subarachnoid haemorrhage before, during and after carotid artery surgery, prolonged cardiopulmonary bypass during heart surgery, head injuries, cardiac arrest: (during arrest and recirculation), aortic surgery, spinal cord ischaemia, severe hypoxia/hypoxaemia, severe hypoperfusion/shock conditions. Although these clinical conditions are markedly different, they share the major similarities of cell death and its pathophysiology and pathogenesis, to which lies the therapy of CNS ischaemia is aimed. New cytoprotective drugs for neuronal damage are lazaroids. The 21-aminosteroids are known as inhibitors of lipid membrane peroxidation which preserve post-injural Ca2+ homeostasis (after total and focal ischaemia). During the last few years evidence has been accumulated about CCAs brain protection against cerebral ischaemia by a virtue of direct neuronal action. The excitatory amino acid antagonists, barbiturates, corticosteroids, antiepileptic drugs and antioxidants complete the cytoprotective treatment possibilities in situations of reduced oxygen supply for CNS. (Ref. 17.)

Animals↗