Recently there has been concern regarding the use of flunitrazepam and other low-dose benzodiazepines in drug-facilitated sexual assault. These compounds are placed in drinks of unsuspecting victims and produce a sedative effect with anterorgrade amnesia. Chip-based microfluidic systems can provide a quick and disposable procedure for the detection of flunitrazepam and other nitrated benzodiazepines used in these crimes. This paper describes the application of indirect quenching of cyanine dye (Cy5) for detection of nitrated benzodiazepines. The separation is performed on a microfluidic device with a separation channel 8 cm long and 50 microm wide and utilizes indirect fluorescence detection with 635 nm laser excitation. The optimization of the separation using micellar electrokinetic chromatography with organic modifiers is described. A borate buffer containing 2.6 microM Cy5 dye, 15 mM sodium dodecyl sulphate (SDS) and 20% methanol is used. Complete separation of four target drugs occurs in under 2 min with limits of detection in the low microg/ml range. Overall the method provides a rapid and simple analysis for the presence of nitrated benzodiazepines in beverages and other similar preparations.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.chroma.2007.05.004 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
UV induced sulfamethazine and carbamazepine elimination in the presence of nitrate: Roles of reactive species and generation risk of highly toxic DBPs.
Sci Total Environ
October 2023
College of Civil Engineering, Zhejiang University of Technology, Hangzhou 310023, China; Zhejiang Key Laboratory of Civil Engineering Structures & Disaster Prevention and Mitigation Technology, Hangzhou 310023, China. Electronic address:
This study systematically compared the degradation kinetics, conversion pathways, formation of disinfection by-products (DBPs), and changes in toxicity for sulfamethazine and carbamazepine in UV/nitrate system. Additionally, the study simulated the generation of DBPs in the post-chlorination process after the introduction of bromine ions (Br). The contributions of UV irradiation, hydroxyl radicals (OH), and reactive nitrogen species (RNS) to SMT degradation were determined to be 28.
View Article and Find Full Text PDFHepatic Encephalopathy and Astrocyte Senescence.
J Clin Exp Hepatol
September 2018
Clinic for Gastroenterology, Hepatology and Infectious Diseases, Heinrich-Heine-University, Düsseldorf, Germany.
Hepatic Encephalopathy (HE) is a severe complication of acute or chronic liver diseases with a broad spectrum of neurological symptoms including motor disturbances and cognitive impairment of different severity. Contrary to former beliefs, a growing number of studies suggest that cognitive impairment may not fully reverse after an acute episode of overt HE in patients with liver cirrhosis. The reasons for persistent cognitive impairment in HE are currently unknown but recent observations raise the possibility that astrocyte senescence may play a role here.
View Article and Find Full Text PDFInhibition of glutamate/glutamine cycle in vivo results in decreased benzodiazepine binding and differentially regulated GABAergic subunit expression in the rat brain.
Epilepsia
August 2010
Institute of Neuroscience and Medicine (INM-2), Research Center Jülich, Jülich, Germany.
Purpose: The astrocytic enzyme glutamine synthetase (GS) is a key regulator of glutamate and γ-aminobutyric acid (GABA) metabolism in the glutamate/glutamine cycle (GGC). Inhibition of GS results in changes of neurotransmitter release and recycling. However, little is known about the influence of GGC on neurotransmitter receptor expression.
View Article and Find Full Text PDFAltered glial-neuronal crosstalk: cornerstone in the pathogenesis of hepatic encephalopathy.
Neurochem Int
November 2010
Neuroscience Research Unit, St-Luc Hospital (CHUM), University of Montreal, Montreal, QC, Canada.
Hepatic encephalopathy (HE) is a serious neuropsychiatric complication of liver failure, characterized neuropathologically by astrocyte swelling, microglial activation and Alzheimer Type II astrocytosis. Molecular studies in HE brain reveal altered expression of genes coding for key astroglial proteins including early losses of expression of GFAP and the glutamate transporter EEAT-2 with concomitant increases of the astrocytic/microglial mitochondrial benzodiazepine receptor (MBR). Decreased expression of EAAT-2 results in decreased glutamate transport and impaired cycling of glutamate-glutamine between astrocytes and neurons, as well as increased extracellular glutamate, activation of the NMDA receptor-mediated cGMP-NO signal transduction pathway, and nitration of tyrosine residues on key astroglial proteins such as glutamine synthetase (GS) and the MBR.
View Article and Find Full Text PDFRNA oxidation and zinc in hepatic encephalopathy and hyperammonemia.
Metab Brain Dis
March 2009
Heinrich-Heine-Universität Düsseldorf, Klinik für Gastroenterologie, Hepatologie, und Infektiologie, Moorenstrasse 5, D-40225 Düsseldorf, Germany.
Article Synopsis
- Hepatic encephalopathy is a cognitive disorder arising from liver failure, primarily driven by increased ammonia levels that lead to swelling of astrocytes in the brain.
- This swelling results in a cycle where reactive oxygen and nitrogen species further exacerbate astrocyte swelling, potentially causing neurotoxic effects and impairing brain functions.
- New findings suggest that astrocyte swelling also leads to RNA oxidation and increased free zinc levels, which may disrupt neurotransmitter systems and gene expression, contributing to cognitive deficits in affected individuals.
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!