Thioacetamide
Liver Cirrhosis, Experimental
Acetamides
Drug-Induced Liver Injury
Liver
Carbon Tetrachloride
Hepatic Stellate Cells
Ethylenethiourea
Schisandra
Amides
Cytochrome P-450 CYP2E1
Liver Cirrhosis
Necrosis
Hepatic Encephalopathy
Evaluation of oxidative stress based on lipid hydroperoxide, vitamin C and vitamin E during apoptosis and necrosis caused by thioacetamide in rat liver. (1/196)
After 12 h of thioacetamide (500 mg/kg body weight) administration to rats, the activity of caspase-3-like protease in the liver increased significantly compared to that in the control group. In plasma, the activity of caspase-3 was barely detectable in the control rat, but had increased significantly after 24 h of drug administration along with a dramatic increase in GOT. These results indicate that thioacetamide causes apoptosis in the liver by activating caspase-3, which is released to plasma by successive necrosis. At 24 h, the concentration of liver lipid hydroperoxides, a mediator of radical reaction, was 2.2 times as high as that of control rats. After 12 and 24 h of thioacetamide administration, the liver concentrations of vitamins C and E decreased significantly. The decrease of antioxidants and formation of lipid hydroperoxides 24 h after thioacetamide administration support the view that extensive radical reactions occur in the liver during the necrotic process. (+info)Potentiation of thioacetamide liver injury in diabetic rats is due to induced CYP2E1. (2/196)
Thioacetamide (TA)-induced hepatotoxicity is potentiated in streptozotocin (STZ)-induced diabetic rats. The relative roles of CYP2E1 and FMO1 in the mechanism of TA-associated liver injury were investigated. In the STZ-induced diabetic rat, hepatic CYP2E1 protein concentration and p-nitrophenol hydroxylation were induced 8- and 5.6-fold, respectively. Pretreatment with the CYP2E1 inducer, isoniazid (INH, 250 mg/kg, i.p.) before TA (300 mg/kg, i.p.) administration significantly increased TA-associated liver injury as assessed by plasma alanine aminotransferase (ALT). Hepatic CYP2E1 expression and p-nitrophenol hydroxylation were induced 2.2- and 2. 5-fold in the INH-pretreated rat, respectively. Inhibition of CYP2E1 by diallyl sulfide (DAS, 200 mg/kg, p.o., two doses) before TA administration, decreased plasma ALT activity by 60% in the nondiabetic rat and by 75% in the diabetic rat. Abolition of microsomal p-nitrophenol hydroxylation and CCl(4)-induced liver injury confirmed that hepatic CYP2E1 was highly inhibited by DAS. Hepatic flavin-containing monooxygenase (FMO) form 1 expression and methimazole-dependent oxidation of thiocholine were induced 2.5- and 1.8-fold in the diabetic rat, respectively. Dietary administration of 0.25% indole-3-carbinol (I3C) for 10 days inhibited FMO1 expression and enzyme activity in both nondiabetic and diabetic rats. Paradoxically, TA-induced liver injury was increased in these I3C-pretreated rats. These findings indicate that hepatic CYP2E1 appears to be primarily involved in bioactivation of TA. In the STZ-induced diabetic rat, diabetes-induced CYP2E1 appears to be responsible for the potentiated liver injury; Even though hepatic FMO1 is induced in the diabetic rat, it is unlikely to mediate the potentiated TA hepatotoxicity. (+info)Non-peptidic analogs of the cell adhesion motif RGD prevent experimental liver injury. (3/196)
In chronic viral hepatitis, autoimmune hepatitis, and some chronic cholestatic liver diseases, T lymphocytes serve as effector cells of the immunostimulatory processes. Cellular interactions of immune cells with extracellular matrix components are regulated primarily via the beta 1 subfamily of integrin receptors. The target epitope of several such integrin receptors is the Arg-Gly-Asp sequence, a cell adhesion motif shared by several matrix-associated adhesive glycoproteins. We review the use of synthetic non-peptidic analogs of RGD in the prevention of immune-mediated, concanavalin A-induced liver damage in mice and in inhibiting the development of liver cirrhosis in rats. The Con A-induced elevation of serum transaminases and tumor necrosis factor-alpha and the infiltration of liver tissue by inflammatory cells were inhibited by pretreatment of the mice with the synthetic RGD mimetics. In rats, the progression of thioacetamide-induced liver cirrhosis was markedly inhibited by the co-administration of the RGD mimetic SF-6,5. The compounds described here may be examined therapeutically for pathological conditions in the liver, manifested as necro-inflammation and fibrosis. (+info)Inducers of gamma-glutamylcysteine synthetase and their effects on glutathione synthetase expression. (4/196)
Synthesis of GSH occurs via two enzymatic steps, the first is catalyzed by gamma-glutamylcysteine synthetase (GCS) and the second is catalyzed by GSH synthetase (GS). A heavy (HS) and light subunit (LS) make up GCS; regulation of both subunits have been well characterized, whereas regulation of GS is largely unknown. In this study, we examined the effects of treatments known to influence the gene expression of GCS subunits on GS expression. Insulin and hydrocortisone treatment of rat hepatocytes or ethanol-feeding of rats for 9 weeks, which increased the expression of GCS-HS only, had no influence on GS expression. However, two-thirds partial hepatectomy in rats which increased the expression of GCS-HS only, also increased GS expression. Treatment of hepatocytes or rats with diethyl maleate, buthionine sulfoximine, tert-butylhydroquinone, or thioacetamide, which increased the expression of both GCS subunits, increased the expression of GS. The GSH synthesis capacity increased 50-100% by treatments that increased only the GCS-HS expression, whereas it increased 161-200% by treatments that increased both GCS-HS and GS expression. Thioacetamide treatment of Chang cells increased cell GSH and GS expression by 50%, but had minimal influence on GCS subunits. Thus, GS induction can further increase the cell's GSH synthetic capacity and in some cells may be as important as GCS in determining the rate of GSH synthesis. (+info)Liver regeneration induced by a designer human IL-6/sIL-6R fusion protein reverses severe hepatocellular injury. (5/196)
The cytokine IL-6 plays a significant role in liver regeneration in conjunction with additional growth factors (HGF, TNF-alpha, and TGF-alpha). Many IL-6 effects depend on a naturally occurring soluble IL-6 receptor (sIL-6R). Here, the chimeric protein hyper-IL-6, constructed from the human IL-6 protein fused to a truncated form of its receptor, was found to have superagonistic IL-6 properties, and as such, enhanced liver cell regeneration. Hyper-IL-6 reversed the state of hepatotoxicity and enhanced the survival rates of rats suffering from fulminant hepatic failure after D-galactosamine administration. The hyper-IL-6 protein has a significant potential for use in the treatment of severe human liver diseases. (+info)Epidermal growth factor reduces multiorgan failure induced by thioacetamide. (6/196)
BACKGROUND: Multiorgan failure is a severe life threatening state where present therapeutic approaches are suboptimal. Epidermal growth factor (EGF) is a potent stimulant of repair in in vitro and in vivo models. We therefore examined its potential beneficial effect in reducing mortality and injury induced by the noxious agent thioacetamide (TAA). METHODS: Mice (20 per group) were fasted overnight and received a single intraperitoneal dose of human recombinant EGF at 10 or 30 microg/kg or saline (control). Either 30 minutes before or after EGF, all animals also received TAA (40 mg/kg intraperitoneally). Twenty four hours later, surviving animals were killed, tissues collected, and degree of organ injury assessed. RESULTS: Fifty per cent (10/20) of control animals died within the first 24 hour period. Mortality was almost completely prevented by the higher dose of EGF whether given before or after TAA (p<0.01) and was reduced by about 50% with the lower dose of EGF. In control animals, the entire length of the jejunum and ileum had necrosis with or without mucosal denudation. In contrast, necrosis affected only about 10-20% of the total length in EGF treated groups (both p<0.01 v control). Control animals showed marked glomerular tuft collapse, interstitial haemorrhage, and increased plasma creatinine levels. These effects were significantly reduced in animals given EGF (30 microg/kg; p<0.01). All groups showed similar changes in liver histology (centrilobular necrosis) and alanine transaminase levels (10-fold increase). CONCLUSIONS: Although EGF did not prevent the hepatotoxicity associated with TAA, it reduced mortality, renal injury, and gastrointestinal damage. These studies provide preliminary evidence that EGF may be a novel approach for the prevention and/or treatment of multiorgan failure. (+info)Restitutive response of Mini rat liver to injury induced by a single oral administration of thioacetamide. (7/196)
Mini rats are a transgenic rat strain carrying antisense gene for rat growth hormone (GH), resulting in retarded growth and a lower blood GH level (136 +/- 42.0 ng/mL) compared with that of age-matched parental strain Wistar rats (329 +/- 337 ng/mL). Mini rats have been used by several investigators as a GH deficiency model. In this work, we gave a single oral administration of thioacetamide (TAA), a hepatotoxicant, to both Mini rats and Wistar rats to ascertain the influence of GH deficiency on liver response to chemically induced injury and subsequent regeneration. TAA administration caused liver injury in both strains, with a greater extent of injury in Mini rats. Proliferation of bile epithelial cells and so-called oval cells was prominent at Day 3 in Mini rats only, and this change correlated well with serum total bilirubin concentrations. Antibody against Ki-67 antigen revealed that cellular proliferation after TAA-induced liver injury was suppressed but prolonged in the Mini rat liver. Although hepatic stellate cells and Kupffer cells/macrophages were more abundant in the livers of TAA-treated Mini rats, the hepatic expression patterns of hepatocyte growth factor and transforming growth factor beta 1 were comparable to those of Wistar rats. Insulin-like growth factor-I gene expression was significantly reduced in the Mini rat liver. Our results imply that a lower GH level may exacerbate chemically induced liver injury, enhance infiltration/proliferation of non-parenchymal cells, suppress regeneration of hepatocytes, and induce proliferation of bile epithelial cells and oval cells when the liver is injured by TAA. (+info)Altered remodeling of nucleolar machineries in cultured hepatocytes treated with thioacetamide. (8/196)
Thioacetamide (TA) is converted into a hyperacetylating agent which causes hepatic necrosis, regeneration, cirrhosis and cancerous transformation. One of the most characteristic toxicities of TA in rat is observed with a 50 mg/kg per day which induces nucleolar enlargement different from that in regenerating liver. From TA-treated liver, the nucleoli were isolated and characterized for an altered nucleolar signal transduction system. Immunochemistry revealed that the poisoned nucleoli had increased levels of both nucleolus specific proteins (nucleophosmin and nucleolin) and various signal molecules (CK2, Erk1/2, p38, protein kinases A and C, and cyclin A). Using flow cytometry, the nucleoli were found to be in G2-arrested nuclei. Manifestation of the nucleolar enlargement could be readily observed using an ex vivo hepatocyte culture. There were two types of nucleolar enlargement. One was observed in normal hepatocytes with light density of enlarged nucleoli. The other was in TA-treated hepatocytes with dense and compact density of enlarged nucleoli, which contained a 3 to 5-fold higher nudeophosmin content than the control. In vitro induction of nucleolar enlargement with TA was possible. As soon as the hepatocytes anchored on a collagen coat, exogeneous TA (higher than 1 microg/mL) could induce dense and compact nucleoli. However, when an exogeneous drug was added after monolayer formation (1 day), no drug-induced nucleolar enlargement was observed. (+info)Thioacetamide is not a medical term, but a chemical compound with the formula TAA or CH3CSNH2. It's used in research and industry, and can be harmful or fatal if swallowed, inhaled, or absorbed through the skin. It can cause damage to the eyes, skin, respiratory system, and digestive tract, and may be harmful to the liver and kidneys with long-term exposure.
However, in a medical context, thioacetamide is sometimes used as a laboratory animal model of hepatotoxicity (liver toxicity) because it can cause centrilobular necrosis (death of cells in the center of liver lobules) and other liver damage when given repeatedly in small doses.
Experimental liver cirrhosis refers to a controlled research setting where various factors and substances are intentionally introduced to induce liver cirrhosis in animals or cell cultures. The purpose is to study the mechanisms, progression, potential treatments, and prevention strategies for liver cirrhosis. This could involve administering chemicals, drugs, alcohol, viruses, or manipulating genes associated with liver damage and fibrosis. It's important to note that results from experimental models may not directly translate to human conditions, but they can provide valuable insights into disease pathophysiology and therapeutic development.
Acetamides are organic compounds that contain an acetamide functional group, which is a combination of an acetyl group (-COCH3) and an amide functional group (-CONH2). The general structure of an acetamide is R-CO-NH-CH3, where R represents the rest of the molecule.
Acetamides are found in various medications, including some pain relievers, muscle relaxants, and anticonvulsants. They can also be found in certain industrial chemicals and are used as intermediates in the synthesis of other organic compounds.
It is important to note that exposure to high levels of acetamides can be harmful and may cause symptoms such as headache, dizziness, nausea, and vomiting. Chronic exposure has been linked to more serious health effects, including liver and kidney damage. Therefore, handling and use of acetamides should be done with appropriate safety precautions.
Drug-Induced Liver Injury (DILI) is a medical term that refers to liver damage or injury caused by the use of medications or drugs. This condition can vary in severity, from mild abnormalities in liver function tests to severe liver failure, which may require a liver transplant.
The exact mechanism of DILI can differ depending on the drug involved, but it generally occurs when the liver metabolizes the drug into toxic compounds that damage liver cells. This can happen through various pathways, including direct toxicity to liver cells, immune-mediated reactions, or metabolic idiosyncrasies.
Symptoms of DILI may include jaundice (yellowing of the skin and eyes), fatigue, abdominal pain, nausea, vomiting, loss of appetite, and dark urine. In severe cases, it can lead to complications such as ascites, encephalopathy, and bleeding disorders.
The diagnosis of DILI is often challenging because it requires the exclusion of other potential causes of liver injury. Liver function tests, imaging studies, and sometimes liver biopsies may be necessary to confirm the diagnosis. Treatment typically involves discontinuing the offending drug and providing supportive care until the liver recovers. In some cases, medications that protect the liver or promote its healing may be used.
I apologize for the confusion, but "Arsenamide" is not a recognized medical term or a medication in modern medicine. It's possible that it may have been used in historical context, but I cannot find any reliable sources that support its use as a medical treatment. Arsenic compounds have been used in medicine in the past, but due to their high toxicity, they are no longer in use today. If you have more information or context about this term, I'd be happy to help further if I can.
The liver is a large, solid organ located in the upper right portion of the abdomen, beneath the diaphragm and above the stomach. It plays a vital role in several bodily functions, including:
1. Metabolism: The liver helps to metabolize carbohydrates, fats, and proteins from the food we eat into energy and nutrients that our bodies can use.
2. Detoxification: The liver detoxifies harmful substances in the body by breaking them down into less toxic forms or excreting them through bile.
3. Synthesis: The liver synthesizes important proteins, such as albumin and clotting factors, that are necessary for proper bodily function.
4. Storage: The liver stores glucose, vitamins, and minerals that can be released when the body needs them.
5. Bile production: The liver produces bile, a digestive juice that helps to break down fats in the small intestine.
6. Immune function: The liver plays a role in the immune system by filtering out bacteria and other harmful substances from the blood.
Overall, the liver is an essential organ that plays a critical role in maintaining overall health and well-being.
Ergothioneine is a naturally occurring antioxidant compound that is found in various foods such as mushrooms, some types of beans, and certain grains. It is also produced by some bacteria that live in the human body. Ergothioneine has been shown to have potential health benefits due to its antioxidant properties, which help protect cells from damage caused by free radicals. Some studies suggest that ergothioneine may have neuroprotective effects and could play a role in preventing neurodegenerative diseases such as Parkinson's and Alzheimer's. However, more research is needed to fully understand the potential health benefits of this compound.
Carbon tetrachloride is a colorless, heavy, and nonflammable liquid with a mild ether-like odor. Its chemical formula is CCl4. It was previously used as a solvent and refrigerant, but its use has been largely phased out due to its toxicity and ozone-depleting properties.
Inhalation, ingestion, or skin contact with carbon tetrachloride can cause harmful health effects. Short-term exposure can lead to symptoms such as dizziness, headache, nausea, and vomiting. Long-term exposure has been linked to liver and kidney damage, as well as an increased risk of cancer.
Carbon tetrachloride is also a potent greenhouse gas and contributes to climate change. Its production and use are regulated by international agreements aimed at protecting human health and the environment.
Liver regeneration is the ability of the liver to restore its original mass and function after injury or surgical resection. This complex process involves the proliferation and differentiation of mature hepatocytes, as well as the activation and transdifferentiation of various types of stem and progenitor cells located in the liver. The mechanisms that regulate liver regeneration include a variety of growth factors, hormones, and cytokines, which act in a coordinated manner to ensure the restoration of normal liver architecture and function. Liver regeneration is essential for the survival of individuals who have undergone partial hepatectomy or who have suffered liver damage due to various causes, such as viral hepatitis, alcohol abuse, or drug-induced liver injury.
Hepatic stellate cells, also known as Ito cells or lipocytes, are specialized perisinusoidal cells located in the space of Disse in the liver. They play a crucial role in maintaining the normal architecture and function of the liver. In response to liver injury or disease, these cells can become activated and transform into myofibroblasts, which produce extracellular matrix components and contribute to fibrosis and scarring in the liver. This activation process is regulated by various signaling pathways and mediators, including cytokines, growth factors, and oxidative stress. Hepatic stellate cells also have the ability to store vitamin A and lipids, which they can release during activation to support hepatocyte function and regeneration.
Ethylenethiourea is defined as a white, crystalline solid with a slightly bitter taste and an odorless property. It is used as a stabilizer in certain industrial processes and products, such as rubber and pesticides. In the medical field, ethylenethiourea has been studied for its potential effects on human health.
It is known to have reproductive and developmental toxicity, and it has been classified as a possible human carcinogen by some organizations. However, exposure to ethylenethiourea through consumer products or the environment is generally low, and the risk it poses to human health is considered to be minimal.
It's important to note that this compound should be handled with care in industrial settings due to its potential hazards. As with any chemical, it's essential to follow proper safety protocols and guidelines when working with ethylenethiourea or any products containing it.
Schisandra is not typically defined in the context of medicine as it refers to a type of plant, rather than a specific medical condition or treatment. Schisandra is a genus of plants that includes several species commonly known as "schisandra" or "schizandra." The most well-known species is Schisandra chinensis, also known as Wu Wei Zi in Traditional Chinese Medicine.
Schisandra chinensis fruits, also called "magnolia vine berries," have been used in traditional medicine systems, including Traditional Chinese Medicine (TCM) and Ayurveda, for centuries. In TCM, schisandra is often referred to as a "five-flavor fruit" because its taste is said to incorporate all five flavors recognized in TCM: sour, bitter, sweet, pungent, and salty.
Schisandra fruits contain various bioactive compounds, including lignans, which have been studied for their potential health benefits. Some research suggests that schisandra extracts may possess antioxidant, anti-inflammatory, hepatoprotective (liver-protecting), and adaptogenic properties. However, more rigorous scientific studies are needed to confirm these findings and establish recommended dosages and safety guidelines for human consumption.
An amide is a functional group or a compound that contains a carbonyl group (a double-bonded carbon atom) and a nitrogen atom. The nitrogen atom is connected to the carbonyl carbon atom by a single bond, and it also has a lone pair of electrons. Amides are commonly found in proteins and peptides, where they form amide bonds (also known as peptide bonds) between individual amino acids.
The general structure of an amide is R-CO-NHR', where R and R' can be alkyl or aryl groups. Amides can be classified into several types based on the nature of R and R' substituents:
* Primary amides: R-CO-NH2
* Secondary amides: R-CO-NHR'
* Tertiary amides: R-CO-NR''R'''
Amides have several important chemical properties. They are generally stable and resistant to hydrolysis under neutral or basic conditions, but they can be hydrolyzed under acidic conditions or with strong bases. Amides also exhibit a characteristic infrared absorption band around 1650 cm-1 due to the carbonyl stretching vibration.
In addition to their prevalence in proteins and peptides, amides are also found in many natural and synthetic compounds, including pharmaceuticals, dyes, and polymers. They have a wide range of applications in chemistry, biology, and materials science.
Cytochrome P-450 CYP2E1 is a specific isoform of the cytochrome P-450 enzyme system, which is involved in the metabolism of various xenobiotics and endogenous compounds. This enzyme is primarily located in the liver and to some extent in other organs such as the lungs, brain, and kidneys.
CYP2E1 plays a significant role in the metabolic activation of several procarcinogens, including nitrosamines, polycyclic aromatic hydrocarbons, and certain solvents. It also contributes to the oxidation of various therapeutic drugs, such as acetaminophen, anesthetics, and anticonvulsants. Overexpression or induction of CYP2E1 has been linked to increased susceptibility to chemical-induced toxicity, carcinogenesis, and alcohol-related liver damage.
The activity of CYP2E1 can be influenced by various factors, including genetic polymorphisms, age, sex, smoking status, and exposure to certain chemicals or drugs. Understanding the regulation and function of this enzyme is crucial for predicting individual susceptibility to chemical-induced toxicities and diseases, as well as for optimizing drug therapy and minimizing adverse effects.
Liver cirrhosis is a chronic, progressive disease characterized by the replacement of normal liver tissue with scarred (fibrotic) tissue, leading to loss of function. The scarring is caused by long-term damage from various sources such as hepatitis, alcohol abuse, nonalcoholic fatty liver disease, and other causes. As the disease advances, it can lead to complications like portal hypertension, fluid accumulation in the abdomen (ascites), impaired brain function (hepatic encephalopathy), and increased risk of liver cancer. It is generally irreversible, but early detection and treatment of underlying causes may help slow down its progression.
Necrosis is the premature death of cells or tissues due to damage or injury, such as from infection, trauma, infarction (lack of blood supply), or toxic substances. It's a pathological process that results in the uncontrolled and passive degradation of cellular components, ultimately leading to the release of intracellular contents into the extracellular space. This can cause local inflammation and may lead to further tissue damage if not treated promptly.
There are different types of necrosis, including coagulative, liquefactive, caseous, fat, fibrinoid, and gangrenous necrosis, each with distinct histological features depending on the underlying cause and the affected tissues or organs.
Hepatic encephalopathy (HE) is a neuropsychiatric syndrome associated with liver dysfunction and/or portosystemic shunting. It results from the accumulation of toxic substances, such as ammonia and inflammatory mediators, which are normally metabolized by the liver. HE can present with a wide range of symptoms, including changes in sleep-wake cycle, altered mental status, confusion, disorientation, asterixis (flapping tremor), and in severe cases, coma. The diagnosis is based on clinical evaluation, neuropsychological testing, and exclusion of other causes of cognitive impairment. Treatment typically involves addressing the underlying liver dysfunction, reducing ammonia production through dietary modifications and medications, and preventing further episodes with lactulose or rifaximin therapy.
Carcinogens are agents (substances or mixtures of substances) that can cause cancer. They may be naturally occurring or man-made. Carcinogens can increase the risk of cancer by altering cellular DNA, disrupting cellular function, or promoting cell growth. Examples of carcinogens include certain chemicals found in tobacco smoke, asbestos, UV radiation from the sun, and some viruses.
It's important to note that not all exposures to carcinogens will result in cancer, and the risk typically depends on factors such as the level and duration of exposure, individual genetic susceptibility, and lifestyle choices. The International Agency for Research on Cancer (IARC) classifies carcinogens into different groups based on the strength of evidence linking them to cancer:
Group 1: Carcinogenic to humans
Group 2A: Probably carcinogenic to humans
Group 2B: Possibly carcinogenic to humans
Group 3: Not classifiable as to its carcinogenicity to humans
Group 4: Probably not carcinogenic to humans
This information is based on medical research and may be subject to change as new studies become available. Always consult a healthcare professional for medical advice.
Thioacetamide
Acetamide
Thiazole
Carleton Moore
Flavin-containing monooxygenase
N,N'-Methylenebisacrylamide
Thioamide
Gustducin
Jatrorrhizine
Sirius Red
Fibrosis
Ubiquitin B
HL156A
Willgerodt rearrangement
Qualitative inorganic analysis
List of MeSH codes (D02)
IARC group 2B
Hydrogen sulfide
TAM
Thioacetamide - Wikipedia
2-(2-Chlorophenoxy)thioacetamide
Metabolism and Toxicity of Thioacetamide and Thioacetamide SOxide in Rat Hepatocytes
THIOACETAMIDE SOLUTION | Reagent for Organic Chemistry | Article No. 6260D
Halofuginone to prevent and treat thioacetamide-induced liver fibrosis in rats
Inhibitory effect of Solanum nigrum on thioacetamide-induced liver fib - Best Ayurveda
Curcumin & Hepatoprotective Focused Research | GreenMedInfo.com
Endocannabinoids affect neurological and cognitive function in thioacetamide-induced hepatic encephalopathy in mice<...
Dietary oxidized frying oil activates hepatic stellate cells and accelerates the severity of carbon tetrachloride- and...
Protective effect of MDL28170 against thioacetamide-induced acute liver failure in mice - Fingerprint - National Yang Ming...
Hepatoprotective effect of Anisotes trisulcus on Thioacetamide-induced Hepatic Cirrhosis in Male Albino Mice, IJSR, Call for...
Marta Méndez - NeL.edu
Data Source Search | MeSH
Murine model to study brain, behavior and immunity during hepatic encephalopathy
Data Source Search | SGCOxCompounds
Nutrients | Free Full-Text | Molecular Bases Underlying the Hepatoprotective Effects of Coffee
Cryzl1 (crystallin zeta like 1) - Rat Genome Database
Ccdc180 (coiled-coil domain containing 180) - Rat Genome Database
Chemical substances, group B - Arbetsmiljöverket
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Thioamides | Profiles RNS
Pungapung / Amorphophallus paeoniifolius / elephant foot yam: Philippine Medicinal Herbs / Philippine Alternative Medicine
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Rats8
- The predominant ECM protein synthesized by the HSC is collagen type I. we evaluated the effect of halofuginone - an inhibitor Of collagen synthesis - on thioacetamide (TAA)-induced liver fibrosis in rats. (agri.gov.il)
- Increased cytochrome oxidase activity in adrenal glands of thioacetamide-cirrhotic rats. (nel.edu)
- Cytochrome oxidase activity has been determined in the adrenal glands of thioacetamide (TAA)-cirrhotic rats. (nel.edu)
- This study aimed to evaluate the effects of TQ on spatial memory and hippocampal long-term potentiation (LTP) in rats with thioacetamide (TAA)-induced liver injury and hepatic encephalopathy. (magiran.com)
- Carnosine Reduces Oxidative Stress and Reverses Attenuation of Righting and Postural Reflexes in Rats with Thioacetamide-Induced Liver Failure. (nih.gov)
- The extract was gavaged daily to the rats, at doses of 100 and 200 mg/kg along with thioacetamide at a dose of 200 mg/kg twice weekly. (ijp-online.com)
- and bilirubin were measured, together with morphological and histopathological indices in the liver of healthy and thioacetamide-treated rats. (ijp-online.com)
- Vitamin D inhibits proliferation and profibrotic marker expression in hepatic stellate cells and decreases thioacetamide-induced liver fibrosis in rats. (springer.com)
Hepatotoxin2
- This study was conducted to determine the effect of ethanolic extract of the dried stems of Tinospora crispa in a male rat model of hepatic fibrosis caused by the hepatotoxin, thioacetamide. (ijp-online.com)
- Initial in vivo studies demonstrated that mice deficient in Cx32, the primary gap junction protein in the liver, were far less susceptible than wild-type mice to actual liver damage and inflammation caused by treatment with the hepatotoxin thioacetamide (TAA). (genengnews.com)
Hepatic encephalopathy1
- Its administration in rat induces hepatic encephalopathy, metabolic acidosis, increased levels of transaminases, abnormal coagulopathy, and centrilobular necrosis, which are the main features of the clinical chronic liver disease so thioacetamide can precisely replicate the initiation and progression of human liver disease in an experimental animal model. (wikipedia.org)
Mice2
- The purpose of this study was to investigate the effects of Solanum nigrum extract (SNE) on thioacetamide (TAA)-induced liver fibrosis in mice. (bestayurveda.ca)
- Mice received two consecutive intraperitoneal injections of thioacetamide (TAA) at low dosage (300 mg/kg). (wjgnet.com)
Hepatocytes1
- Metabolism and Toxicity of Thioacetamide and Thioacetamide S-Oxide in Rat Hepatocytes. (ku.edu)
Acute1
- Thioacetamide is known to induce acute or chronic liver disease (fibrosis and cirrhosis) in the experimental animal model. (wikipedia.org)
Formula1
- Thioacetamide is an organosulfur compound with the formula C2H5NS. (wikipedia.org)
Mouse2
- We used a mouse model of a thioacetamide induced fulminant hepatic failure. (tau.ac.il)
- In both carbon tetrachloride (CCl 4 )- and thioacetamide (TAA)-induced liver fibrosis mouse models, we showed that long-term administration of a 10% fried oil-containing diet significantly upregulated fibrogenesis genes expression and deposition of hepatic collagen. (tmu.edu.tw)
Solution1
- Thus, treatment of aqueous solutions of many metal cations to a solution of thioacetamide affords the corresponding metal sulfide: M2+ + CH3C(S)NH2 + H2O → MS + CH3C(O)NH2 + 2 H+ (M = Ni, Pb, Cd, Hg) Related precipitations occur for sources of soft trivalent cations (As3+, Sb3+, Bi3+) and monovalent cations (Ag+, Cu+). (wikipedia.org)
Protects against thioacetamide-induced3
- Tranilast reduces serum IL-6 and IL-13 and protects against thioacetamide-induced acute liver injury and hepatic encephalopathy. (ugm.ac.id)
- Melatonin inhibits nuclear factor kappa B activation and oxidative stress and protects against thioacetamide induced liver damage in rats. (ugm.ac.id)
- 7. Pyrrolidine dithiocarbamate protects against thioacetamide-induced fulminant hepatic failure in rats. (nih.gov)
Hepatotoxicity4
- Effect of an antimitotic agent colchicine on thioacetamide hepatotoxicity. (nih.gov)
- Ipomoea aquatica extract shows protective action against thioacetamide-induced hepatotoxicity. (ugm.ac.id)
- 3. Curcumin ameliorates acute thioacetamide-induced hepatotoxicity. (nih.gov)
- The hepatotoxicity and neurotoxicity marker genes were further validated using additional hepatotoxic (thioacetamide, dimethylnitrobenzene and carbon tetrachloride) or neurotoxic (ethyl parathion, chlorpyrifos and malathion) chemicals. (cdc.gov)
Hepatic1
- Its administration in rat induces hepatic encephalopathy, metabolic acidosis, increased levels of transaminases, abnormal coagulopathy, and centrilobular necrosis, which are the main features of the clinical chronic liver disease so thioacetamide can precisely replicate the initiation and progression of human liver disease in an experimental animal model. (wikipedia.org)
Extract1
- Molecular Changes Following Induction of Hepatocellular Carcinoma by Diethylnitrosamine and Thioacetamide, and Subsequent Treatment with Dioscorea membranacea Extract. (nih.gov)
Acid1
- 14. Treatment of thioacetamide-induced liver cirrhosis by the Ras antagonist, farnesylthiosalicylic acid. (nih.gov)
Journal1
- Synthesis and Characterization of Cadmium-Thioacetamide Nanocomposites Using a Facile Sonochemical Approach: A precursor for Producing CdS Nanoparticles via Thermal Decomposition', International Journal of Nanoscience and Nanotechnology , 9(4), pp. 203-212. (ijnnonline.net)
Study1
- An overview of Genetic Toxicology Mammalian Cell Mutagenicity study conclusions related to Thioacetamide (62-55-5). (nih.gov)