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PubMed2003

Cytisine binds with similar affinity to nicotinic alpha4beta2 receptors on the cell surface and in homogenates.

Cytisine and nicotine bound to specific sites in homogenates prepared from HEK 293 cells which stably express human neuronal nicotinic alpha4 and beta2 subunits. The number of sites was the same for both ligands and nicotine was a full competitive inhibitor of cytisine binding. However, when binding was done to intact cells the number of binding sites per cell for nicotine was approximately 4-fold the number of sites for cytisine. Nicotine fully blocked cytisine binding, but cytisine only partially blocked nicotine binding to intact cells. When cells were permeabilized with saponin, the number of sites for nicotine was unchanged, while the number of sites for cytisine was increased, and cytisine was able to fully block nicotine binding. These data indicate that cytisine binds only to surface receptors on intact cells. The apparent affinity of cytisine for surface receptors (K(d)=0.8 nM) was not significantly different from that for receptors in the cell homogenate (0.3 nM).

Alkaloids↗
PubMed2003

Pharmacological characterization of dopamine, norepinephrine and serotonin release in the rat prefrontal cortex by neuronal nicotinic acetylcholine receptor agonists.

Neuronal nicotinic acetylcholine receptors (nAChRs) modulate synaptic transmission by regulating neurotransmitter release, an action that involves multiple nAChRs. The effects of four nAChR agonists, nicotine (NIC), 1,1-dimethyl-4-phenylpiperzinium iodide (DMPP), cytisine (CYT) and epibatidine (EPI) were investigated on [3H]-norepinephrine (NE), [3H]-dopamine (DA) and [3H]-serotonin (5-HT) release from rat prefrontal cortical (PFC) slices. All four agonists evoked [3H]-DA release to a similar magnitude but with a differing rank order of potency of EPI>>DMPP approximately NIC approximately CYT. Similarly, all four agonists also increased [3H]-NE release, but with a differing rank order of potency of EPI>>CYT approximately DMPP>NIC. NIC-induced [3H]-NE and [3H]-DA release responses were both calcium-dependent and attenuated by the sodium channel antagonist, tetrodotoxin (TTX) and by the nAChR antagonists mecamylamine (MEC) and dihydro-beta-erythroidine (DHbetaE), but not by D-tubocurare (D-TC). The modulation of [3H]-5-HT release by nAChR agonists was distinct from that seen for catecholamines. DMPP produced robust increases with minimal release observed with other agonists. DMPP-induced [3H]-5-HT release was neither sensitive to known nAChR antagonists nor dependent on external calcium. The differences between nicotinic agonist induced catecholamine and serotonin release suggest involvement of distinct nAChRs.

Alkaloids↗
PubMed1997

Cognitive impairment in spontaneously hypertensive rats: role of central nicotinic receptors. I.

Both human essential hypertension and genetically induced hypertension in rats have been associated with a range of impairments of cognitive ability. The spontaneous hypertensive rat (SHR) previously has been shown to exhibit a decrease in the expression of brain nicotinic acetylcholine receptors, a factor that could play a role in the impaired ability of this strain in the performance of learning and memory-related tasks. The purpose of this study was to help determine whether task impairment by SHR was related to the reduced expression of central nicotinic acetylcholine receptors. Twelve-week-old SHR were tested in two phases of a water maze (spatial memory) task, and their performance was compared with that of two age-matched normotensive strains, Wistar Kyoto (WKY) and Wistar rats. During Phase 1, SHR exhibited significantly increased latencies to locate a hidden platform as compared with either WKY or Wistar rats. During Phase 2 (subsequent series of trials after a 4-day inter-phase period), where rats were required to find a new platform location, SHR again exhibited significantly impaired performance compared to the normotensive strains. In a single trial passive avoidance paradigm, SHR again displayed significantly reduced avoidance behavior as compared with both WKY and Wistar rats. In consecutive coronal sections, the density of [3H]cytisine binding sites was decreased in SHR by up to 25% in about half of the brain regions examined, with the deficits particularly apparent in cephalic regions. The binding of [125I]alpha-bungarotoxin to brain sections also was decreased in SHR; however, only certain brain areas exhibited significant interstrain differences. These alterations in the expression of putative nicotinic receptor subtypes in SHR were not due to changes in the density of cholinergic neurons since there were no interstrain differences in the binding densities for [3H]vesamicol, which labels the vesicular acetylcholine transporter. Moreover, the magnitude of nicotine-stimulated rubidium efflux from cortical and striatal synaptosomes in vitro was significantly reduced in samples derived from SHR as compared with those from normotensive rats. These results are consistent with the possibility that a reduction in the expression of cortical nicotinic receptors in SHR plays a role in this strain's impaired performance of both spatial and non-spatial learning and memory-related tasks.

Alkaloids↗
PubMed1997

Cognitive impairment in spontaneously hypertensive rats: role of central nicotinic receptors. Part II.

The adult spontaneously hypertensive rat (SHR) has been shown to exhibit a decrease in the expression and nicotine-stimulated function of brain nicotinic acetylcholine receptors, factors that could play a role in the impaired ability of this strain in the performance of learning and memory-related tasks. The purpose of this study was to determine whether either or both the impaired task performance and the loss of nicotinic receptors is directly related to the presence of the hypertensive state. To address this issue, two experimental approaches were taken. In the first series, 4-week-old pre-hypertensive SHR were tested in two phases of a water maze (spatial memory) task, and their performance was compared with that of two age-matched normotensive strains, Wistar Kyoto (WKY) and Wistar rats. During phase 1, SHR and WKY rats were not different in their ability to learn the task. In contrast, during phase 2 (subsequent series of trials after a 4 day inter-phase period), where rats were required to find a new platform location, SHR exhibited significantly impaired performance compared to both WKY and Wistar normotensive controls. In a single trial passive avoidance paradigm, SHR again displayed significantly reduced avoidance behavior as compared with both WKY and Wistar rats. In consecutive coronal sections the density of [3H]cytisine binding sites was decreased in pre-hypertensive SHR by up to 18% in about 40% of the brain regions examined, with the deficits particularly apparent in frontal cortex (layers 4-6), posterior subiculum, several thalamic regions, and the interpeduncular nucleus. In the second series, age-matched SHR and WKY were treated with the antihypertensive agent hydralazine administered in the drinking water beginning at 4 weeks of age. Hydralazine prevented the development of hypertension in adult SHR, but did not forestall the reduced expression of brain nicotinic receptors, nor the impairment in learning- and memory-related tasks normally observed in untreated adults with established hypertension. Moreover, the magnitude of nicotine-stimulated rubidium efflux from cortical and striatal synaptosomes in vitro was significantly reduced in samples derived from hydralazine-treated SHR as compared with those from hydralazine-treated, or untreated WKY. These results support the contention that the hypertensive state does not directly contribute to the reduced expression of nicotinic receptors in SHR. Therefore, the SHR may provide an important genetic model for the study of the role of central nicotinic receptors in cognitive and learning abnormalities.

Aging↗
PubMed1998

Stimulation of alpha4beta2 nicotinic acetylcholine receptors inhibits beta-amyloid toxicity.

We examined the effects of nicotinic receptor agonists against beta amyloid (Abeta) cytotoxicity to rat cortical neurons. Administration of nicotine protected against Abeta-induced neuronal death. This neuroprotection was blocked by dihydro-beta-erythroidine, an alpha4beta2 nicotinic receptor antagonist. Furthermore, incubation with cytisine, a selective alpha4beta2 nicotinic receptor agonist, inhibited Abeta cytotoxicity. These results suggest that alpha4beta2 nicotinic receptor activation plays an important role in neuroprotection against Abeta cytotoxicity.

Alkaloids↗
PubMed1999

Inducible, heterologous expression of human alpha7-nicotinic acetylcholine receptors in a native nicotinic receptor-null human clonal line.

Tetracycline-regulated expression of recombinant nicotinic acetylcholine receptors (nAChR) composed of human alpha7 subunits is achieved in native nAChR-null SH-EP1 human epithelial cells. alpha7 subunits are heterologously expressed as messenger RNA and as components of 125I-labeled alpha-bungarotoxin (I-Bgt)-binding nAChR ( approximately 10 pmol per milligram of membrane protein) at levels sensitive to the amount of tetracycline in cell growth medium. I-Bgt-binding alpha7-nAChR appear on the cell surface pool and in intracellular pools. The pharmacological profile for drug competition toward I-Bgt binding to these recombinant alpha7-nAChR matches that of human native alpha7-nAChR naturally expressed in SH-SY5Y human neuroblastoma cells (rank order potency methyllycaconitine>1, 1-dimethyl-4-phenylpiperazinium>(-)nicotine>cytisine>carbamylch oli ne> /=d-tubocurarine). Chronic exposure to nicotine induces up-regulation of human recombinant alpha7-nAChR (80% up-regulation at 10 microM nicotine) just as it does native alpha7-nAChR in other human cell lines. These studies confirm expression of nAChR as homooligomers of human alpha7 subunits from transgenes, establish a native nAChR-null background for such expression, and demonstrate that this expression can be regulated to facilitate studies of human alpha7-nAChR.

Acetylcholine↗
PubMed1999

Adolescent nicotine exposure causes persistent upregulation of nicotinic cholinergic receptors in rat brain regions.

Whereas numerous studies have explored the consequences of fetal or adult nicotine exposure, little or no basic research has been conducted for nicotine exposure during adolescence, the developmental period in which regular cigarette use typically begins. We administered nicotine to adolescent rats on postnatal days 30-47 via continuous infusion with implanted osmotic minipumps, using a dose rate (3-6 mg kg-1 day-1) set to achieve plasma nicotine levels found in smokers; results were compared to exposure of adult rats. During and after exposure, we assessed nicotinic cholinergic receptor binding in the midbrain, cerebral cortex, and hippocampus, using [3H]cytisine. Robust receptor upregulation was observed with both adolescent and adult nicotine exposure but there were major differences in the regional specificity and persistence of effect. In adolescents, upregulation was uniform across all regions during the infusion period, whereas in adults, there was a distinct regional hierarchy: midbrain < cerebral cortex < hippocampus; accordingly, receptors in the adolescent midbrain were upregulated far more than with adult exposure. In addition, adolescent nicotine treatment produced long-lasting effects on the receptors, with significant increases still apparent in male rats 1 month after the termination of drug exposure. We also obtained evidence for hippocampal cell damage in adolescent female rats exposed to nicotine, characterized by increases in total membrane protein concentration indicative of a decrease in overall cell size. Adolescent nicotine exposure thus elicits region- and gender-selective effects that differ substantially from those in adults, effects that may contribute to increased addictive properties and lasting deficits in behavioral performance.

Age Factors↗
PubMed2000

Antiparkinson potential of delta-opioid receptor agonists.

delta-Opioid receptors, present in very high concentrations in striatum and overlying cortex, are thought to be involved in a number of processes, including analgesia, mood, reward, modulation of neuronal excitability, and alterations in neurotransmitter release. Given the localization of the receptors in motor circuits in brain, we thought it of interest to study the antiparkinson potential of delta-opioid receptor agonists. Rats were given unilateral 6-hydroxydopamine lesions of the nigrostriatal tract, and following recovery, were tested for rotational activity. Tonazocine mesylate is a nonpeptide, partial delta-opioid receptor agonist with mu-receptor antagonist properties. Tonazocine (0.1-10 mg/kg) evoked a dose-related, ipsilateral rotation, consistent with augmentation of dopaminergic function on the unlesioned side. The rotation evoked by tonazocine was blocked by the selective delta-opioid receptor antagonist naltrindole, suggesting that the effect was mediated by delta-opioid receptors. The full delta-opioid receptor agonist (+)-4-¿9-alpha-R)-alpha-(2S,5RO-4-allyl-2, 5-dimethyl-1-piperaziny l)-3-methoxybenzyl-N,N-diethylbenzamide (SNC-80) produced both contralateral and ipsilateral rotation. Tonazocine additionally augmented the effects of L-3,4 dihydroxyphenylalanine (L-DOPA) on reserpine-induced suppression of motor activity. Binding affinities and efficacies of tonazocine and SNC-80 against mu-, kappa-, and delta-opioid receptors were also confirmed and compared to standards. These data suggest therapeutic potential of agents interacting with delta-opioid receptors, and indicate some differences in the activities of tonazocine and SNC-80.

Animals↗
PubMed2003

Blockade of nicotine-induced locomotor sensitization by a novel neurotensin analog in rats.

Neurotensin is a tridecapeptide with anatomic and functional relationships to dopaminergic neurons. Previously we showed that one of our brain-penetrating neurotensin analogs, NT69L (N-met-L-Arg, L-Lys, L-Pro, L-neo-Trp, L-tert-Leu, L-Leu), blocks cocaine- and D-amphetamine-induced hyperactivity in rats. We have now performed a similar study in rats sensitized to nicotine over 15 days of administration. Male Sprague-Dawley rats were randomly assigned to receive daily injections for 15 days with one of the following combinations: saline/nicotine (0.35 mg/kg), NT69L (1 mg/kg)/nicotine, saline/saline, or NT69L/saline with a 30-min period between injections. On day 15 each group was given saline/nicotine or NT69L/nicotine and tested in an activity chamber. One-time administration of NT69L attenuated nicotine-induced activity with an ED(50) of 1.6 microg/kg. Rats injected with nicotine over the 15 days had a significant increase in locomotor activity, consistent with nicotine-induced locomotor sensitization. A single injection of NT69L on day 15 prior to nicotine markedly decreased nicotine-induced hyperactivity. Although daily injections of NT69L lessened its effect, statistically significant reductions in hyperactivity to nicotine persisted throughout the study. There was no significant difference in activity between rats injected with NT69L/saline and saline/saline. Thus, the activity reduction was not due to sedation. Acute and chronic nicotine injection caused an increase in cytisine binding in prefrontal cortex. NT69L significantly reduced the increase caused by acute but not chronic injection of nicotine. Nicotine injection resulted in an increase in dopamine levels in the striatum and dopamine and norepinephrine levels in the prefrontal cortex. NT69L lowered the norepinephrine and dopamine levels in the prefrontal cortex but did not affect striatal dopamine. The present study is the first report, to our knowledge, of a possible role for neurotensin in the development of nicotine dependence, and suggests that neurotensin analogs such as NT69L may be explored as treatment for nicotine and other psychostimulant abuse.

Alkaloids↗
PubMed2003

Nitrogen substitution modifies the activity of cytisine on neuronal nicotinic receptor subtypes.

Cytisine very potently binds and activates the alpha 3 beta 4 and alpha 7 nicotinic subtypes, but only partially agonises the alpha 4 beta 2 subtype. Although with a lower affinity than cytisine, new cytisine derivatives with different substituents on the basic nitrogen (CC1-CC8) bind to both the heteromeric and homomeric subtypes, with higher affinity for brain [3H]epibatidine receptors. The cytisine derivatives were tested on the Ca(2+) flux of native or transfected cell lines expressing the rat alpha 7, or human alpha 3 beta 4 or alpha 4 beta 2 subtypes using Ca(2+) dynamics in conjunction with a fluorescent image plate reader. None elicited any response at doses of up to 30-100 microM, but all inhibited agonist-induced responses. Compounds CC5 and CC7 were also electrophysiologically tested on oocyte-expressed rat alpha 4 beta 2, alpha 3 beta 4 and alpha 7 subtypes. CC5 competitively antagonised the alpha 4 beta 2 and alpha 3 beta 4 subtypes with similar potency, whereas CC7 only partially agonised them with maximum responses of respectively 3% and 11% of those of 1 mM acetylcholine. Neither compound induced any current in the oocyte-expressed alpha 7 subtype, and both weakly inhibited acetylcholine-induced currents. Adding chemical groups of a different class or size to the basic nitrogen of cytisine leads to compounds that lose full agonist activity on the alpha 3 beta 4 and alpha 7 subtypes.

Alkaloids↗
PubMed1998

Pharmacological characterization of nicotinic receptor-mediated acetylcholine release in rat brain--an in vivo microdialysis study.

In vivo microdialysis was used to investigate nicotinic receptor-mediated acetylcholine release in the hippocampus, frontal cortex, and striatum of freely moving rats. Intraperitoneal administration of (-)-nicotine increased the release of acetylcholine in the hippocampus and frontal cortex but not in the striatum. (-)-Nicotine exhibited a bell-shaped dose-response relationship, and showed attenuation of response at the highest dose (5.0 mg/kg i.p.) in both the hippocampus and frontal cortex. In the hippocampus, (-)-nicotine (1.0 mg/kg i.p.)-induced increase of acetylcholine release was blocked by pretreatment with the centrally acting nicotinic receptor channel blocker, mecamylamine (1.0 mg/kg i.p.), but not by hexamethonium (5.0 mg/kg i.p.), suggesting that the effects of (-)-nicotine were mediated by the central nicotinic receptor. (S)-3-methyl-5-(1-methyl-2-pyrrolidinyl)isoxazole (ABT-418, 1.0 and 5.0 mg/kg i.p.), reported to be a selective agonist for alpha4beta2 nicotinic receptor subunits, also enhanced the release of acetylcholine in the hippocampus, while 3-(2,4-dimethoxybenzlidene)-anabaseine (GTS-21, 1.0 and 5.0 mg/kg i.p.), which has high affinity for the alpha7 nicotinic receptor subunit, was without effect. The natural alkaloids isolated from plants, (-)-cytisine and (-)-lobeline, had little effect on acetylcholine release from the hippocampus. A competitive antagonist for alpha4beta2 subunits of the nicotinic receptor, dihydro-beta-erythroidine, and a partial agonist for the beta2 subunit-containing nicotinic receptor, (-)-cytisine, inhibited (-)-nicotine-induced increase of acetylcholine release from the hippocampus, whereas a selective antagonist for the alpha7 subunit, methyllycaconitine, and a partial agonist for the alpha3 subunit-containing nicotinic receptor, (-)-lobeline, did not. These results indicate that there are certain differences among brain regions in the response of nicotinic receptor-mediated acetylcholine release and that (-)-nicotine-induced acetylcholine release in the rat hippocampus may be attributed to activation of the alpha4beta2 nicotinic receptor subunits.

Acetylcholine↗
PubMed1998

Effects of cytisine on hydroxyl radicals in vitro and MPTP-induced dopamine depletion in vivo.

The potential new iron-chelator cytisine and the radical scavenger N-tert-butyl-alpha-(2-sulfophenyl) nitrone (S-PBN) were incubated in a Fenton system and hydroxyl radical formation was measured with the salicylate trapping assay. Both cytisine and S-PBN reduced hydroxyl radical formation in a concentration-dependent manner. For in vivo studies, C57BL/6 mice were injected repeatedly with cytisine (0.5 mg/kg or 2.0 mg/kg s.c.) or saline seven days before and after a single 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) injection (30 mg/kg s.c.). Seven days after MPTP treatment alone dopamine levels were significantly reduced to 12% of the control values (p < 0.001), whereas MPTP + cytisine treatment (2 mg/kg) led to more than twofold higher dopamine levels (p < 0.01) compared with MPTP alone. We have shown for the first time that cytisine attenuates hydroxyl radical formation in vitro and reduces MPTP-induced dopamine depletion. Thus, cytisine may be useful for the treatment of Parkinson's Disease where the chelation of iron ions could prevent neuronal cell death.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1980

A morphometric study of the pulmonary Clara cell in normal and nitrosoheptamethyleneimine-treated European hamsters.

Previous studies have identified the bronchial Clara cell as the progenitor of the lung tumors induced in European hamsters by nitrosoheptamethyleneimine (NHMI). Using stereological methods, we compared the ultrastructure of Clara cells from untreated animals and lung tumor cells, induced by NHMI, in the European hamster. The composition and volume of the cytoplasm was significantly altered in the tumor cells whereas the nuclei did not show any measurable changes in size or structure when compared with the controls.

Animals↗
PubMed2002

Cytisine derivatives as high affinity nAChR ligands: synthesis and comparative molecular field analysis.

A number of new N-substituted cytisine derivatives were prepared and tested, along with similar compounds already described by us and others, as high affinity neuronal acetylcholine receptor ligands. Structure-affinity relationships were discussed in the light of our recently proposed pharmacophore model for nicotinic receptor agonists. The most significant physicochemical interactions modulating the receptor-ligand binding were detected at the three dimensional (3D) level by means of comparative molecular field analysis (CoMFA). The best predictive PLS model was a single-field steric model showing good statistical figures: n = 17, Q2 = 0.717, s(ev) = 0.566, r2 = 0.942, s = 0.275.

Alkaloids↗
PubMed2003

Cytisine derivatives as ligands for neuronal nicotine receptors and with various pharmacological activities.

Neuronal nicotinic acetylcholine receptors (nAChRs) form a family of ACh-gated cation channels made up of different subtypes. They are widely distributed in peripheral and central nervous systems and are involved in complex cerebral processes as learning, memory, nociception, movement, etc. The possibility that subtype-selective ligands be used in the treatment of CNS disorders promoted the synthesis of a large number of structural analogues of nicotine and epibatidine, two very potent nAChR agonists. Pursuing our long standing research on the structural modification of quinolizidine alkaloids, we devoted our attention to cytisine, another very potent ligand for many nAChR subtypes. Thus a systematic structural modification of cytisine was undertaken in order to obtain compounds of potential therapeutic interest at peripheral as well as central level, with a particular concern for achieving nAChR subtype selective ligands. Up to the present more than 80 cytisine derivatives, mainly of N-substitution and a few by modifying the pyridone ring, have been prepared. The biological results, which concern so far about an half of the prepared compounds, indicate that the introduction of a nitro group in position 3 of the pyridone nucleus further enhances the high affinity of cytisine, while the introduction of substituents on the basic nitrogen, though reducing in different degrees the affinity, gives rise to compounds with a higher selectivity for central (alpha(4)beta(2)) versus gangliar (alpha(3)-containing) receptor subtype. On the other hand, the analgesic, antihypertensive and inotropic activities found in some N-substituted cytisines, represent an attractive starting point for the development of more active compounds.

Alkaloids↗
PubMed1999

Synthesis and preliminary pharmacological evaluation of some cytisine derivatives.

Thirty-one N-derivatives of cytisine were prepared in order to modify its pharmacological profile and to obtain compounds of potential therapeutic interest either at a peripheral or central level, particularly as nicotinic ligands with improved ability to cross the blood-brain barrier. Actually, with the introduction of different kinds of substituent on the basic nitrogen of cytisine a variety of activities were observed, both in vivo (analgesic, dopamine antagonism, antihypertensive, inhibition of stress-induced ulcers, antiinflammatory, protection from PAF-induced mortality, hypoglycemic) and in vitro (positive cardio-inotropic, beta-adrenergic antagonism, alpha 1- and alpha 2-antagonism, inhibition of PAF-induced platelet aggregation). Six randomly selected compounds were tested for the ability to recognize a central nicotinic receptor and four of them exhibited Ki values in the range 30-163 nM.

Adrenergic alpha-2 Receptor Antagonists↗
PubMed2001

Detection of the cyclic nitramine explosives hexahydro-1,3,5-trinitro- 1,3,5-triazine (RDX) and octahydro- 1,3,5,7-tetranitro- 1,3,5,7-tetrazine (HMX) and their degradation products in soil environments.

The cyclic nitramine explosives hexahydro-1,3,5-trinitro-1,3,5-triazine (RDX) and octahydro-1,3,5,7-tetranitro-1,3,5,7-tetrazine (HMX) were examined in field and microcosm soil samples to determine their patterns of degradation and environmental fates. A number of analytical techniques, including solid-phase microextraction with on-fiber derivatization, gas chromatography-mass spectrometry, gas chromatography with electron-capture detection, liquid chromatography-mass spectrometry, and micellar electrokinetic chromatography were required for the analyses. Two different classes of intermediates were detected, both of which lead ultimately to the formation of nitrous oxide (N2O) and carbon dioxide (CO2). The first class was identified as the nitroso derivatives formed by the sequential reduction of -NO2 functional groups. The second class of intermediates, which was favored at higher humidities and in the presence of anaerobic sludge amendments, consisted of ring cleavage products including bis-(hydroxymethyl)-nitramine and methylenedinitramine. Rye-grass (Lolium perenne) present in field samples was found to extract and accumulate HMX from soil without further degradation. In all cases (excepting the plant samples), the indigenous microbes or amended domestic anaerobic sludge consortia degraded the cyclic nitramine explosives eventually to produce N2O and CO2.

Azocines↗
PubMed2002

Detection of explosives and their degradation products in soil environments.

Polynitro organic explosives [hexahydro-1,3,5-trinitro-1,3,5-triazine (RDX), octahydro-1,3,5,7-tetranitro-1,3,5,7-tetrazocine (HMX) and 2,4,6-trinitrotoluene (TNT)] are typical labile environmental pollutants that can biotransform with soil indigenous microorganisms, photodegrade by sunlight and migrate through subsurface soil to cause groundwater contamination. To be able to determine the type and concentration of explosives and their (bio)transformation products in different soil environments, a comprehensive analytical methodology of sample preparation, separation and detection is thus required. The present paper describes the use of supercritical carbon dioxide (SC-CO2), acetonitrile (MeCN) (US Environmental Protection Agency Method 8330) and solid-phase microextraction (SPME) for the extraction of explosives and their degradation products from various water, soil and plant tissue samples for subsequent analysis by either HPLC-UV, capillary electrophoresis (CE-UV) or GC-MS. Contaminated surface and subsurface soil and groundwater were collected from either a TNT manufacturing facility or an anti-tank firing range. Plant tissue samples were taken fromplants grown in anti-tank firing range soil in a greenhouse experiment. All tested soil and groundwater samples from the former TNT manufacturing plant were found to contain TNT and some of its amino reduced and partially denitrated products. Their concentrations as determined by SPME-GC-MS and LC-UV depended on the location of sampling at the site. In the case of plant tissues, SC-CO2 extraction followed by CE-UV analysis showed only the presence of HMX. The concentrations of HMX (<200 mg/kg) as determined by supercritical fluid extraction (SC-CO2)-CE-UV were comparable to those obtained by MeCN extraction, although the latter technique was found to be more efficient at higher concentrations (>300 mg/kg). Modifiers such as MeCN and water enhanced the SC-CO2 extractability of HMX from plant tissues.

Azocines↗