CDIA™ Tetrodotoxin Colloidal Gold Test Cassette is a lateral flow chromatographic immunoassay for the detection of TTX in environmental swabs or sea water.
Storage
The kit can be stored at room temperature (4-30°C). The test kit is stable through the expiration date (12 months). DO NOT FREEZE. Do not store the test kit in direct sunlight.
Sensitivity
1.5ppm(μg/g)
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. Compared to the traditional method, the developed colloidal gold nanoparticle probe for the immunoassay is rapid and accuracy, and the detection can be finished in several minutes.
Citations
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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. Traditional methods for detecting TTX, such as LC-MS or HPLC, have limitations due to the lack of commercially available standards, making analysis challenging. However, Creative Diagnostics has developed a Tetrodotoxin Colloidal Gold Test Cassette, which is a competitive lateral flow immunochromatographic assay. This test offers high sensitivity and specificity in detecting TTX without the need for additional reagents or equipment. It serves as a valuable tool in research settings, providing an efficient and accessible method for TTX detection.
Alternative Names
Tetrodotoxin (TTX) Colloidal Gold Test Cassette TTX Colloidal Gold Test Cassette Tetrodotoxin (TTX) Lateral Flow Detection Kit
References
1. Nieto F R, et al. Tetrodotoxin (TTX) as a therapeutic agent for pain. Marine Drugs. 2012, 10(2): 281-305.
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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.
Development of ELISA and colloidal gold immunoassay for tetrodotoxin detetcion based on monoclonal antibody
A monoclonal hybridoma cell named 5B9 against tetrodotoxin (TTX) was obtained after fusion of myeloma SP2/0 cells with spleen cells isolated from the immunized Balb/c mice. The 5B9 monoclonal antibody (McAb) with high affinity (about 2.55×109) is specific to TTX, and this McAb belongs to the immunoglobulin G (IgG) isotype. Finally, an enzyme-linked immunosorbent assay (ELISA) and colloidal gold immunoassay were established based on this McAb. The linear range of ELISA to detect TTX was 5–500 ng/mL, and the limit of detection (LOD) was 4.44 ng/mL. The average CV of intra- and inter-assay was less than 8%, with the samples recovery range of 70.93–99.99%. A competitive format colloidal gold strip was developed for detection of TTX in real samples, and the LOD for TTX is 20 ng/mL, and the assay time of the qualitative test can be finished in less than 10 min without any equipment. The result from test strip revealed that the test strip has a good agreement with those obtained from ELISA.
Non-genomic action of vitamin D3 on N-methyl-D-aspartate and kainate receptor-mediated actions in juvenile gonadotrophin-releasing hormone neurons
REPRODUCTION FERTILITY AND DEVELOPMENT
Authors: Bhattarai, Pravin; Bhattarai, Janardhan P.; Kim, Min Sun; Han, Seong Kyu
Vitamin D is a versatile signalling molecule that plays a critical role in calcium homeostasis. There are several studies showing the genomic action of vitamin D in the control of reproduction; however, the quick non-genomic action of vitamin D at the hypothalamic level is not well understood. Therefore, to investigate the effect of vitamin D on juvenile gonadotrophin-releasing hormone (GnRH) neurons, excitatory neurotransmitter receptor agonists N-methyl-D-aspartate (NMDA, 30M) and kainate (10M) were applied in the absence or in the presence of vitamin D3 (VitaD3, 10nM). The NMDA-mediated responses were decreased by VitaD3 in the absence and in the presence of tetrodotoxin (TTX), a sodium-channel blocker, with the mean relative inward current being 0.56 +/- 0.07 and 0.66 +/- 0.07 (P<0.05), respectively. In addition, VitaD3 induced a decrease in the frequency of gamma-aminobutyric acid mediated (GABAergic) spontaneous postsynaptic currents and spontaneous postsynaptic currents induced by NMDA application with a mean relative frequency of 0.595 +/- 0.07 and 0.56 +/- 0.09, respectively. Further, VitaD3 decreased the kainate-induced inward currents in the absence and in the presence of TTX with a relative inward current of 0.64 +/- 0.06 and 0.68 +/- 0.06, respectively (P<0.05). These results suggest that VitaD3 has a non-genomic action and partially inhibits the NMDA and kainate receptor-mediated actions of GnRH neurons, suggesting that VitaD3 may regulate the hypothalamic-pituitary-gonadal (HPG) axis at the time of pubertal development.
Xenin Augments Duodenal Anion Secretion via Activation of Afferent Neural Pathways
JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS
Authors: Kaji, Izumi; Akiba, Yasutada; Kato, Ikuo; Maruta, Koji; Kuwahara, Atsukazu; Kaunitz, Jonathan D.
Xenin-25, a neurotensin (NT)-related anorexigenic gut hormone generated mostly in the duodenal mucosa, is believed to increase the rate of duodenal ion secretion, because xenin-induced diarrhea is not present after Roux-en-Y gastric bypass surgery. Because the local effects of xenin on duodenal ion secretion have remained uninvestigated, we thus examined the neural pathways underlying xenin-induced duodenal anion secretion. Intravenous infusion of xenin-8, a bioactive C-terminal fragment of xenin-25, dose dependently increased the rate of duodenal HCO (3) (-) secretion in perfused duodenal loops of anesthetized rats. Xenin was immunolocalized to a subset of enteroendocrine cells in the rat duodenum. The mRNA of the xenin/NT receptor 1 (NTS1) was predominantly expressed in the enteric plexus, nodose and dorsal root ganglia, and in the lamina propria rather than in the epithelium. The serosal application of xenin-8 or xenin-25 rapidly and transiently increased short-circuit current in Ussing-chambered mucosa-submucosa preparations in a concentration-dependent manner in the duodenum and jejunum, but less so in the ileum and colon. The selective antagonist for NTS1, substance P (SP) receptor (NK1), or 5-hydroxytryptamine (5-HT) (3), but not NTS2, inhibited the responses to xenin. Xenin-evoked Cl-secretion was reduced by tetrodotoxin (TTX) or capsaicin-pretreatment, and abolished by the inhibitor of TTX-resistant sodiumchannel Nav1.8 in combination with TTX, suggesting that peripheral xenin augments duodenal HCO3- and Cl- secretion through NTS1 activation on intrinsic and extrinsic afferent nerves, followed by release of SP and 5-HT. Afferent nerve activation by postprandial, peripherally released xeninmay account for its secretory effects in the duodenum.