PubMed Health⌕ Search

PubMed · 10431363

Capillary electrophoresis with diode array detection as an alternative analytical method for paralytic and amnesic shellfish toxins.

Abstract

In recent years the marine environment has been seriously damaged by the presence of several toxic phytoplanktonic species, such as dinoflagellates and other toxic algae, which contaminate shellfish and other marine products. Amnesic and paralytic shellfish toxins are examples of these contaminants. The search for sensitive methodologies for the analysis of such compounds is one of the aims of researchers working in the marine environment. High-performance liquid chromatographic methods have been used for this purpose, allowing the detection of very low levels of these toxins. Recently, capillary electrophoresis (CE) has been used as an alternative for the separation and analysis of these compounds. In this paper, we report the optimization of CE procedures for their analysis. Due to the complexity of the matrix, clean-up procedures are required for removing interferences which affect the electrophoretic resolution. The influences of electrophoretic parameters such as voltage, buffer concentrations and organic modifiers, were studied in order to optimize the electrophoretic system to achieve high resolution as well as an accurate quantitation. Extraction and other steps such as clean-up of samples prior to the electrophoretic analysis have been also studied. Different buffers and organic modifiers were used in order to improve the separation of the toxic components, and consequently to obtain accurate quantitative information about the amount of toxins present in the contaminated samples.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

N Piñeiro, J M Leão, A Gago Martínez, J A Rodríguez Vázquez. 1999-06-25. Capillary electrophoresis with diode array detection as an alternative analytical method for paralytic and amnesic shellfish toxins.. https://doi.org/10.1016/s0021-9673(99)00428-8

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Amnesia and driving.

Two experienced drivers who developed severe amnesia due to bilateral hippocampal lesions participated in a series of standardized challenges of driving performance and knowledge of driving rules. During drives in a high fidelity simulator and on the road in an instrumented vehicle, they demonstrated vehicle control similar to that of normal drivers on measures of steering, speed control, safety errors, and driving with distraction. Their knowledge of driving rules, safety procedures, and road sign meaning also was normal. However, both participants were impaired at following route directions, and both had unsafe responses in a difficult crash avoidance scenario on the simulator. These findings suggest that memory impairment acquired by experienced drivers does not impair most aspects of driving performance, but may increase safety risk under some challenging circumstances.

Amnesia↗

Determination of the EC50 amnesic concentration of etomidate and its diffusion profile in brain tissue: implications for in vitro studies.

BACKGROUND: Etomidate is a widely used general anesthetic that has become a useful tool to investigate mechanisms of anesthetic action in vivo and in brain slices. However, the free aqueous concentration of etomidate that corresponds to amnesia in vivo and the diffusion profile of etomidate in brain slices are not known. METHODS: The authors assessed the effect of intraperitoneally injected etomidate on contextual fear conditioning in mice. Etomidate concentrations in brain tissue were obtained by high-performance liquid chromatography. Uptake studies in 400-microm-thick brain slices were used to calculate the diffusion and partition coefficients of etomidate. A diffusion model was used to calculate the expected concentration profile within a brain slice as a function of time and depth. The predicted rate of drug equilibration was compared with the onset of electrophysiologic effects on inhibitory circuit function in recordings from hippocampal brain slices. RESULTS: Etomidate impaired contextual fear conditioning with an ED50 dose of 11.0+/-0.1 mg after intraperitoneal injection, which corresponded to an EC50 brain concentration of 208+/-9 ng/g. The brain:artificial cerebrospinal fluid partition coefficient was 3.35, yielding an EC50,amnesia aqueous concentration of 0.25 microm. The diffusion coefficient was approximately 0.2x10 cm/s. The development of etomidate action in hippocampal brain slices was compatible with the concentration profile predicted by this diffusion coefficient. CONCLUSIONS: The free aqueous concentration of etomidate corresponding to amnesia, as defined by impaired contextual fear conditioning in mice, is 0.25 microM. Diffusion of etomidate into brain slices requires approximately an hour to reach 80% equilibration at a typical recording depth of 100 microm. This information will be useful in designing and interpreting in vitro studies using etomidate.

Amnesia↗