AMMONIUM TETRATHIOMOLYBDATE
AMMONIUM TETRATHIOMOLYBDATE
CAS: 15060-55-6
Molecular Formula: (NH4)2MoS4
AMMONIUM TETRATHIOMOLYBDATE - Names and Identifiers
AMMONIUM TETRATHIOMOLYBDATE - Physico-chemical Properties
| Molecular Formula | (NH4)2MoS4 |
| Molar Mass | 260.27 |
| Melting Point | >300 °C (lit.) |
| Water Solubility | Slightly soluble in water. |
| Storage Condition | Room Temprature |
| MDL | MFCD00136013 |
| Use | Use aziridine ring opening to form sulfide and disulfide. |
AMMONIUM TETRATHIOMOLYBDATE - Risk and Safety
| Risk Codes | R20/21/22 - Harmful by inhalation, in contact with skin and if swallowed. R36/37/38 - Irritating to eyes, respiratory system and skin. |
| Safety Description | S26 - In case of contact with eyes, rinse immediately with plenty of water and seek medical advice. S36 - Wear suitable protective clothing. S37/39 - Wear suitable gloves and eye/face protection |
AMMONIUM TETRATHIOMOLYBDATE - Improvement of preparation method of ammonium tetrathiomolybdate
from Wanfang
Author:
Chai Yongming , Zhao Hui-ji , ververververo Liu , Liu Chengguang
Abstract:
ammonium tetrathiomolybdate [(NH4):MoS4] was prepared by the reaction of ammonium sulfide with ammonium molybdate (or molybdenum trioxide), which improved the synthesis process of ammonium tetrathiomolybdate. Quasi-in-situ UV-VIS spectrum and pH meter were used to detect the synthesis process in real time, the results show that S ^ 2-replacing two O ^ 2-in MoO4 ^ 2-to generate MoO2S2 ^ 2-(orange) is extremely fast (<1min), the process of generating Moos 3S ^ 2-(yellow) was not observed, and then the process of generating Moos 3 ^ 2-(orange red) was carried out in the middle with the reaction time extended to about 30min, finally, MoS4 ^ 2-(blood red) was formed, and the pH of the solution decreased gradually with the extension of the reaction time. UV-VIS of the product, XRD and LRS results show that the synthesized ammonium tetrathiomolybdate has high purity and good crystal form.
Key words:
ammonium tetrathiomolybdate; Ammonium sulfide; ammonium molybdate
DOI:
10.3969/j.issn.1006-4990.2007.05.005
cited:
year:
2007
Last Update：2024-01-02 23:10:35
AMMONIUM TETRATHIOMOLYBDATE - Characterization of ammonium tetrathiomolybdate as catalyst precursor in catalytic hydropyrolysis reaction
from hownet
Author:
Zhou Jianwei , Li Zhu-yuan Yue Changtao , Zhong Ningning
Abstract:
by means of thermogravimetric analysis, differential thermal analysis, FT-IR and X-ray diffraction analysis, the catalytic hydrogenation catalyst MoS2 precursor (NH4) the thermal decomposition mechanism and crystal structure of 2MoS4 were studied, and the catalytic pyrolysis performance was also tested. The thermal decomposition of ammonium tetrathiomolybdate is closely related to the heat treatment temperature, and begins to decompose to molybdenum sulfide with catalytic activity above 350 ℃. The catalytic hydropyrolysis experiments were carried out at 550 ℃ in hydrogen atmosphere by using coal samples impregnated with catalyst precursor. Show its catalytic performance.
Key words:
DOI:
10.3969/j.issn.0258-3283.2006.02.008
cited:
year:
2006
Last Update：2023-08-16 22:05:47
AMMONIUM TETRATHIOMOLYBDATE - Study on the mechanism of copper metabolism and MAPK related signal transduction in rats with Wilson's disease
from hownet
Author:
Abstract:
background Wilson disease (WD) is one of the few neurogenetic diseases that can be treated. At present, the metal chelating agent represented by Penicillamine (PCA) has the advantages of high urinary copper excretion and significant improvement of symptoms, but it has many adverse reactions. Zinc and other drugs to reduce copper absorption although fewer adverse reactions, but the role of copper is weak, more for patients with pre-symptoms or maintenance therapy. Therefore, the treatment of WD needs WD drugs with good effect and few side effects. Tetrathiomolybdate (TM) is a chelating agent of copper ions, which is absorbed into the blood and forms a non-toxic three-group complex with albumin and blood copper, competition inhibits the absorption of copper in intestinal mucosa, which can effectively promote the excretion of copper and reduce the concentration of free copper. At present, TM has been reported to be successful in the treatment of WD, and it has been found that it has a certain effect on the damage of liver and brain tissue. Because the drug is still in clinical trials, its specific mechanism of efficacy and adverse reactions is not yet clear. Copper load rat model of liver, kidney tissue can produce similar to WD copper deposition, and has the advantages of low price, good repeatability, easy to obtain, it is a good animal model for studying the pathogenesis and pharmacotherapy of WD. Studies have shown that liver damage is the most common clinical manifestation of WD patients, and liver fibrosis is the most common pathological change. P38, Extracellular regulated protein kinase (ERK),c-jun N-terminal kinase (JNK), C- jun N-terminal kinase, as mitogen activated protein kinase (mitogen activated protein kinase, MAPK) pathway plays an important role in the development of liver fibrosis. Other studies have found that excessive copper can cause free radical damage to nerve cells, activate various intracellular protein and enzyme cascade signals such as MAPK pathway, and regulate transcription factors and gene expression in the nucleus, cause intracellular calcium overload, leading to nerve cell degeneration, necrosis, and on this basis, activation of c-fos,c-jun,c-myc gene expression, induced apoptosis of nerve cells. Whether TM can repair liver and brain tissue damage by regulating MAPK and other signaling pathways on the basis of chelating copper ions has not been reported. Study Objectives 1. To observe the changes of Cu,Zn,Fe,Mo and other trace elements in vivo before and after TM treatment of copper load rats, and to observe the regulation of TM on copper metabolism and other trace elements in copper load rats, and to explore its possible mechanism; 2. Observe the changes of behavior, blood routine, liver and kidney function before and after TM treatment of copper overload rats, observe the curative effect and adverse reaction of TM; 3. To observe the expression levels of P38,ERK,JNK and other proteins in liver and brain tissues of rats before and after TM treatment of copper load, and to explore the mechanism of P38,ERK,JNK and other signaling pathways involved in WD liver and brain injury, and the protective mechanism of TM regulating the above signaling pathways in liver and brain injury, providing experimental theoretical basis for TM treatment of WD. Research Methods 1. A total of 140 SD rats were randomly divided into five groups: normal control group, copper load model Group, TM group, PCA Group and wedou decoction group. The copper overload rat model was established by feeding feed containing 1g/kg copper sulfate and 0.185% copper sulfate water. Normal control group and the same environment as the treatment group, normal feeding, once a day to normal saline 0.2/10g gavage for 4 weeks; the copper load model group was fed with 0.2 copper sulfate water and feed containing 1g/kg copper sulfate once a day for 4 weeks according to 0.185%/10G once a day; TM Group (2 mg/kg once daily) was given TM by gavage for 4 consecutive weeks; PCA Group (0.09 g/kg once daily) was given PCA by gavage for 4 consecutive weeks; chinese medicine group according to 0.2ml/10G once a day to the traditional Chinese medicine liver bean decoction by gavage, for 4 consecutive weeks, observe the behavior of rats in each group and other changes. 2. The contents of Cu,Zn,Fe,Mo and other trace elements in serum, liver tissue and brain tissue of rats in each group before and after treatment were detected by plasma atomic emission spectrometry and plasma mass spectrometry, analysis of the correlation between Mo and Cu and other trace elements; 3. The blood routine, liver and kidney function of rats in each group were detected before and after treatment, and the difference was observed. The curative effect and adverse reaction of TM in the treatment of copper load rats were observed. Application of immunohistochemistry-DAB staining method, Western-Blot method to detect WD copper load rat model before and after treatment of liver, brain tissue P38,ERK,JNK and other protein expression levels, to investigate the regulation of TM on the above pathways and the mechanism of repair of liver and brain injury in WD copper-loaded rats. The effect of TM on copper-related trace element metabolism in copper-loaded rats 1.1 the body weight, coat and mental state of copper-loaded rats were worse than those of normal rats, and were improved after treatment; the serum copper content of 1.2 rats at 12 weeks was significantly higher than that at 4,8,16 weeks (P<0.05), up to nearly 2 times. 1.3 serum trace elements: TM group serum Cu was significantly lower than the model Group (P0.01), compared with PCA Group, Chinese medicine group had no significant change (P0.05); serum Zn was higher than that in model Group (P0.05); Serum Fe was significantly lower than that in PCA Group (P0.01); Serum Mo content in model group was significantly lower than that in normal Group and TM Group (P0.01); serum Se in TM group was significantly higher than that in normal Group and model Group (P0.01). Serum Ni in TM group was higher than that in normal group, model Group and traditional Chinese medicine group (P0.05). 1.4 Trace Elements in liver tissue: the content of Cu in TM group was significantly lower than that in model Group (P0.01), which was slightly lower than that in PCA Group and traditional Chinese medicine group (P0.05); there was no significant change in liver Zn in TM group compared with other groups (P0.05); Liver Fe in TM group was significantly higher than that in other groups (P<0.01); mo content in liver of TM group was significantly higher than that in other groups (P<0.01), and liver Al content in TM group was significantly lower than that in model group (P<0.01);TM group of liver I were significantly higher than other groups (P<0.01);TM group of liver Pb content was significantly lower than the model group (P<0.01); 1.5 brain trace elements: the content of Cu in TM group was significantly lower than that in traditional Chinese medicine group and model Group (P0.05), and the content of Zn in TM group was significantly lower than that in other groups (P0.05); fe content in TM group was significantly lower than that in model group (P<0.01), and Al content in TM group was significantly lower than that in model group (P<0.01); pb content in TM group was significantly lower than that in model Group and traditional Chinese medicine group (P<0.01). The blood routine, liver function and renal function in the 1.6TM group were within the normal range, and there was no significant change compared with the normal group. 2.1 The Expression of P38,ERK and JNK were detected by immunohistochemistry: The positive expression of each protein was Brown, the positive expression of the model group and each treatment group were found, the positive expression of the model group was significantly higher than that of the other groups (P0.01), and the positive expression of each protein in the TM group was higher than that in the PCA Group (P0.05), however, the positive expression of each protein in TM group was lower than that in PCA Group (P0.05). No obvious positive expression of JNK protein in brain tissue. 2.2Western-Blot detection of P38,ERK,JNK protein expression: the protein levels were significantly different between the groups, the positive expression of each protein in the model group was significantly increased (P0.01),TM group, PCA Group, Chinese medicine group compared with the model Group, the relative expression of positive protein decreased significantly (P0.01),TM group compared with the PCA group Positive protein expression increased (P0.05). There was no specific protein band expression of JNK protein in brain tissue. Conclusion 1. Copper load leads to excessive accumulation of copper in liver and brain tissue of rats, and can cause abnormal liver function and abnormal behavior and other manifestations of liver and brain tissue damage. 2. Copper Overload can induce the activation of P38,ERK,JNK and other signaling pathways in rat liver and brain tissue, causing liver and brain cell damage. 3. TM has the effect of improving liver function and behavior of copper loaded rats, and has no adverse reactions such as blood routine, liver and kidney function. 4.TM can reduce the content of Cu in serum, liver and brain tissue of rats with copper load (the effect of removing copper is not significantly different from that of PCA), which is the main reason for improving liver and brain tissue damage. 5. TM treatment of copper load rats after serum Mo and Cu,Zn,Fe content was positively correlated, mo may participate in the regulation of liver cell injury and central nerve cell injury by antagonizing the above trace elements. 6. TM can down regulate the phosphorylation of P38,ERK,JNK and other proteins in the liver and brain of copper loaded rats Level, is an important reason to improve liver and brain tissue damage.
stowed
Key words:
ammonium tetrathiomolybdate copper load trace elements P38 protein ERK protein JNK protein
cited:
Last Update：2023-08-16 22:05:47
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