The Tetrodotoxin indirect competitive ELISA is an immunoassay for the quantitative and sensitive detection of Tetrodotoxin in water samples and puffer fish samples.
Storage
Store the kit at 2- 8°C.The shelf life is 12 months when the kit is properly stored.
Precision
Coefficients of variation (CVs) for standards: <10% CVs for samples: <15%
Detection Range
0-270ng/ml
Sensitivity
≤3.3ng/ml
General Description
Tetrodotoxin (TTX) is a powerful neurotoxin, which is tolerance to heat, salt and cooking. Minimum lethal dose for human is about 0.5mg/60 kg of body weight, the toxicity is 1000 times great than the sodium cyanide. Every year many people are ill due to improper eating or eating puffer fish. Therefore, it is significant to accurate detection of tetrodotoxin in puffer fish in order to prevention and control of tetrodotoxin poisoning. The detection method is sensitive, fast, simple and specific, only need a small amount of fish sampling.
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Background
Tetrodotoxin (TTX) is a potent neurotoxin that is widely recognized for its extreme toxicity. It belongs to a class of toxins known as saxitoxins, and it is primarily found in certain marine organisms, most notably pufferfish (also known as fugu), as well as in some other marine species, such as certain types of octopus, newts, and frogs. TTX is infamous for its ability to cause severe poisoning in humans when ingested. Upon ingestion, TTX rapidly distributes throughout the body, affecting various organs and tissues. Its toxic effects primarily target the nervous system, leading to a range of symptoms including numbness and tingling, weakness, dizziness, nausea, vomiting, respiratory distress, paralysis, and, in severe cases, can lead to respiratory failure and death. Historical investigations of tetrodotoxin poisoning cases have revealed a strong correlation between blood TTX levels and the severity of poisoning symptoms. TTX acts by selectively blocking voltage-gated sodium channels, which are essential for the generation and propagation of action potentials in nerve cells. By binding to specific sites on these channels, TTX prevents the influx of sodium ions, effectively halting the transmission of nerve impulses. This blockade leads to muscle paralysis and can result in respiratory failure and death if the toxin reaches a critical concentration. Despite the serious effects of tetrodotoxin, there is currently no specific antidote or treatment available for TTX intoxication. The primary approach to managing TTX poisoning is through observation and providing appropriate supportive care to alleviate symptoms and prevent complications.
Figure 1. Schematic representation of voltage-gated sodium channel α-subunits and Tetrodotoxin (TTX) binding site. (Source: Nieto, F. R. et al., 2012)
It is significant to accurate detection of tetrodotoxin in puffer fish to prevention and control of tetrodotoxin poisoning. The Tetrodotoxin ELISA Kit is a TTX residue detection product developed using ELISA technology. Compared with instrumental analysis technology, it is fast, simple, accurate, and highly sensitive, and can reduce operating errors and work intensity. This kit allows for the screening of a large number of samples simultaneously, making it suitable for routine monitoring, quality control, and research applications.
Q: I am confused about antibody as my samples (having kappa scFv against TTx) from hamsters. Should I use kit antibody or anti-his as scFv has his tag or anti-kappa.
A: Please refer to the principle of the reagent kit in the instruction manual. If some TTx in the customer's test sample has already bound to the scFv antibody, it may affect the recognition site of our detection antibody, thereby affecting the overall TTx detection. However, in this case, free TTx can still be detected. Therefore, there is no issue with using the kit's antibodies.
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References
An Updated Review of Tetrodotoxin and Its Peculiarities
Marine Drugs
Authors: Katikou P, Gokbulut C, Kosker A R, et al.
Tetrodotoxin (TTX) is a crystalline, weakly basic, colorless organic substance and is one of the most potent marine toxins known. Although TTX was first isolated from pufferfish, it has been found in numerous other marine organisms and a few terrestrial species. Moreover, tetrodotoxication is still an important health problem today, as TTX has no known antidote. TTX poisonings were most commonly reported from Japan, Thailand, and China, but today the risk of TTX poisoning is spreading around the world. Recent studies have shown that TTX-containing fish are being found in other regions of the Pacific and in the Indian Ocean, as well as the Mediterranean Sea. This review aims to summarize pertinent information available to date on the structure, origin, distribution, mechanism of action of TTX and analytical methods used for the detection of TTX, as well as on TTX-containing organisms, symptoms of TTX poisoning, and incidence worldwide.
The development and optimization of ELISA for the determination of tetrodotoxin.
Objective To optimize the ELISA for the determination of tetrodotoxin. Methods A competitive enzyme-linked immunosorbent assay (ELISA) was used. In the ELISA, 100 μl antigen (1.0 μg/ml) was coated on the microtiter plate for 60 min at 37 C or over night at 4 C. The plate was then washed 3 times with PBS-T for 3-5 s each time. The optimal incubation time for monoclonal antibody (mAb), goat anti-mice IgG peroxidase conjugate and OPD were 30 min. 20 min and 10 min at 37 C, respectively. Results The detection limit is 0.05 ng in each well. The curve was linear for TTX doses between 5-5 000 ng/ml (0.25-250 ng for every assay). The linear regress equation was Y = 0.30 88X — 0.17 41 (R. = 0.99 01). The average callback for TTX of muscles and gonads were 99.74% and 100.30%, respectively. The sensitivity of optimization ELISA was 5 times than traditional method and the time of 1.8 h were saved. Conclusion The optimized ELISA is an idealmethod for the determination of tetrodotoxin.
Alfaxalone Causes Reduction of Glycinergic IPSCs, but Not Glutamatergic EPSCs, and Activates a Depolarizing Current in Rat Hypoglossal Motor Neurons
FRONTIERS IN CELLULAR NEUROSCIENCE
Authors: Lau, Cora; Thakre, Prajwal P.; Bellingham, Mark C.
We investigated effects of the neuroactive steroid anesthetic alfaxalone on intrinsic excitability, and on inhibitory and excitatory synaptic transmission to hypoglossal motor neurons (HMNs). Whole cell recordings were made from HMNs in brainstem slices from 7 to 14-day-old Wistar rats. Spontaneous, miniature, and evoked inhibitory post-synaptic currents (IPSCs), and spontaneous and evoked excitatory PSCs (EPSCs) were recorded at -60 mV. Alfaxalone did not alter spontaneous glycinergic IPSC peak amplitude, rise-time or half-width up to 10 mu M, but reduced IPSC frequency from 3 mu M. Evoked IPSC amplitude was reduced from 30 nM. Evoked IPSC rise-time was prolonged and evoked IPSC decay time was increased only by 10 mu M alfaxalone. Alfaxalone also decreased evoked IPSC paired pulse ratio (PPR). Spontaneous glutamatergic EPSC amplitude and frequency were not altered by alfaxalone, and evoked EPSC amplitude and PPR was also unchanged. Alfaxalone did not alter HMN repetitive firing or action potential amplitude. Baseline holding current at -60 mV with a CsCl-based pipette solution was increased in an inward direction; this effect was not seen when tetrodotoxin (TTX) was present. These results suggest that alfaxalone modulates glycine receptors (GlyRs), causing a delayed and prolonged channel opening, as well as causing presynaptic reduction of glycine release, and activates a membrane current, which remains to be identified. Alfaxalone selectively reduces glycinergic inhibitory transmission to rat HMNs via a combination of pre- and post-synaptic mechanisms. The net effect of these responses to alfaxalone is to increase HMN excitability and may therefore underlie neuro-motor excitation during neurosteroid anesthesia.
Tetrodotoxin-Sensitive Sodium Channels Mediate Action Potential Firing and Excitability in Menthol-Sensitive Vglut3-Lineage Sensory Neurons
JOURNAL OF NEUROSCIENCE
Authors: Griffith, Theanne N.; Docter, Trevor A.; Lumpkin, Ellen A.
Small-diameter vesicular glutamate transporter 3-lineage (Vglut3(lineage)) dorsal root ganglion (DRG) neurons play an important role in mechanosensation and thermal hypersensitivity; however, little is known about their intrinsic electrical properties. We therefore set out to investigate mechanisms of excitability within this population. Calcium microfluorimetry analysis of male and female mouse DRG neurons demonstrated that the cooling compound menthol selectively activates a subset of Vglut3(lineage) neurons. Whole-cell recordings showed that small-diameter Vglut3(lineage) DRG neurons fire menthol-evoked action potentials and exhibited robust, transient receptor potential melastatin 8 (TRPM8)-dependent discharges at room temperature. This heightened excitability was confirmed by current-clamp and action potential phase-plot analyses, which showed menthol-sensitive Vglut3(lineage) neurons to have more depolarized membrane potentials, lower firing thresholds, and higher evoked firing frequencies compared with menthol-insensitive Vglut3(lineage) neurons. A biophysical analysis revealed voltage-gated sodium channel (Na-v) currents in menthol-sensitive Vglut3(lineage) neurons were resistant to entry into slow inactivation compared with menthol-insensitive neurons. Multiplex in situ hybridization showed similar distributions of tetrodotoxin (TTX)-sensitive Na-v transcripts between TRPM8-positive and -negative Vglut3(lineage) neurons; however, Na-v 1.8 transcripts, which encode TTX-resistant channels, were more prevalent in TRPM8-negative neurons. Conversely, pharmacological analyses identified distinct functional contributions of Nay subunits, with Na-v 1.1 driving firing in menthol-sensitive neurons, whereas other small-diameter Vglut3(lineage) neurons rely primarily on TTX-resistant Nay channels. Additionally, when Na-v 1.1 channels were blocked, the remaining Nay current readily entered into slow inactivation in menthol-sensitive Vglut3(lineage) neurons. Thus, these data demonstrate that TTX-sensitive Na(v)s drive action potential firing in menthol-sensitive sensory neurons and contribute to their heightened excitability.
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Figure 1. Schematic representation of voltage-gated sodium channel α-subunits and Tetrodotoxin (TTX) binding site.
