A nitrosamine derivative with alkylating, carcinogenic, and mutagenic properties.
Experimentally induced tumors of the LIVER.
A class of compounds that contain a -NH2 and a -NO radical. Many members of this group have carcinogenic and mutagenic properties.
A hepatic carcinogen whose mechanism of activation involves N-hydroxylation to the aryl hydroxamic acid followed by enzymatic sulfonation to sulfoxyfluorenylacetamide. It is used to study the carcinogenicity and mutagenicity of aromatic amines.
An enzyme, sometimes called GGT, with a key role in the synthesis and degradation of GLUTATHIONE; (GSH, a tripeptide that protects cells from many toxins). It catalyzes the transfer of the gamma-glutamyl moiety to an acceptor amino acid.
Substances that increase the risk of NEOPLASMS in humans or animals. Both genotoxic chemicals, which affect DNA directly, and nongenotoxic chemicals, which induce neoplasms by other mechanism, are included.
A barbituric acid derivative that acts as a nonselective central nervous system depressant. It potentiates GAMMA-AMINOBUTYRIC ACID action on GABA-A RECEPTORS, and modulates chloride currents through receptor channels. It also inhibits glutamate induced depolarizations.
Highly reactive chemicals that introduce alkyl radicals into biologically active molecules and thereby prevent their proper functioning. Many are used as antineoplastic agents, but most are very toxic, with carcinogenic, mutagenic, teratogenic, and immunosuppressant actions. They have also been used as components in poison gases.
Pathological processes that tend eventually to become malignant. (From Dorland, 27th ed)
F344 rats are an inbred strain of albino laboratory rats (Rattus norvegicus) that have been widely used in biomedical research due to their consistent and reliable genetic background, which facilitates the study of disease mechanisms and therapeutic interventions.
A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.
The combination of two or more different factors in the production of cancer.
Tumors or cancer of the LIVER.
Diethylamines are organic compounds consisting of two ethyl groups bonded to an amino nitrogen atom, with the general formula (C2H5)2NH, known for their foul odor and use as chemical intermediates in various industrial applications, but notably not associated with medical definitions unless referring to potential substance abuse or intoxication.
Tests to experimentally measure the tumor-producing/cancer cell-producing potency of an agent by administering the agent (e.g., benzanthracenes) and observing the quantity of tumors or the cell transformation developed over a given period of time. The carcinogenicity value is usually measured as milligrams of agent administered per tumor developed. Though this test differs from the DNA-repair and bacterial microsome MUTAGENICITY TESTS, researchers often attempt to correlate the finding of carcinogenicity values and mutagenicity values.
An oxidation product of HEPTACHLOR formed by many plants and animals, including humans, after exposure to HEPTACHLOR. It has been shown to remain in soil treated with HEPTACHLOR for over fifteen years and is toxic to animals and humans. (From ATSDR Public Heath Statement, April 1989)
A transferase that catalyzes the addition of aliphatic, aromatic, or heterocyclic FREE RADICALS as well as EPOXIDES and arene oxides to GLUTATHIONE. Addition takes place at the SULFUR. It also catalyzes the reduction of polyol nitrate by glutathione to polyol and nitrite.
Excision of all or part of the liver. (Dorland, 28th ed)
A nitrosamine derivative with alkylating, carcinogenic, and mutagenic properties. It causes serious liver damage and is a hepatocarcinogen in rodents.
A benign epithelial tumor of the LIVER.
A primary malignant neoplasm of epithelial liver cells. It ranges from a well-differentiated tumor with EPITHELIAL CELLS indistinguishable from normal HEPATOCYTES to a poorly differentiated neoplasm. The cells may be uniform or markedly pleomorphic, or form GIANT CELLS. Several classification schemes have been suggested.
The measurement of an organ in volume, mass, or heaviness.
The only genus in the family Oryziinae, order BELONIFORMES. Oryzias are egg-layers; other fish of the same order are livebearers. Oryzias are used extensively in testing carcinogens.
An insecticide and herbicide that has also been used as a wood preservative. Pentachlorphenol is a widespread environmental pollutant. Both chronic and acute pentachlorophenol poisoning are medical concerns. The range of its biological actions is still being actively explored, but it is clearly a potent enzyme inhibitor and has been used as such as an experimental tool.
Experimentally induced new abnormal growth of TISSUES in animals to provide models for studying human neoplasms.
A condition produced by a deficiency of CHOLINE in animals. Choline is known as a lipotropic agent because it has been shown to promote the transport of excess fat from the liver under certain conditions in laboratory animals. Combined deficiency of choline (included in the B vitamin complex) and all other methyl group donors causes liver cirrhosis in some animals. Unlike compounds normally considered as vitamins, choline does not serve as a cofactor in enzymatic reactions. (From Saunders Dictionary & Encyclopedia of Laboratory Medicine and Technology, 1984)
A very potent liver carcinogen.
An enzyme that catalyzes the conversion of D-glucose 6-phosphate and water to D-glucose and orthophosphate. EC 3.1.3.9.
The covalent bonding of an alkyl group to an organic compound. It can occur by a simple addition reaction or by substitution of another functional group.
Repair or renewal of hepatic tissue.
A carcinogen that is often used in experimental cancer studies.
Agents that reduce the frequency or rate of spontaneous or induced tumors independently of the mechanism involved.
The main structural component of the LIVER. They are specialized EPITHELIAL CELLS that are organized into interconnected plates called lobules.
A nitrosourea compound with alkylating, carcinogenic, and mutagenic properties.
The mass or quantity of heaviness of an individual. It is expressed by units of pounds or kilograms.
Study of intracellular distribution of chemicals, reaction sites, enzymes, etc., by means of staining reactions, radioactive isotope uptake, selective metal distribution in electron microscopy, or other methods.
A fibric acid derivative used in the treatment of HYPERLIPOPROTEINEMIA TYPE III and severe HYPERTRIGLYCERIDEMIA. (From Martindale, The Extra Pharmacopoeia, 30th ed, p986)
Genetically identical individuals developed from brother and sister matings which have been carried out for twenty or more generations or by parent x offspring matings carried out with certain restrictions. This also includes animals with a long history of closed colony breeding.
A nucleoside consisting of the base guanine and the sugar deoxyribose.
Cell changes manifested by escape from control mechanisms, increased growth potential, alterations in the cell surface, karyotypic abnormalities, morphological and biochemical deviations from the norm, and other attributes conferring the ability to invade, metastasize, and kill.
An increase in the number of cells in a tissue or organ without tumor formation. It differs from HYPERTROPHY, which is an increase in bulk without an increase in the number of cells.
A genus of the family Muridae having three species. The present domesticated strains were developed from individuals brought from Syria. They are widely used in biomedical research.
A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.

Assaying potential carcinogens with Drosophila. (1/604)

Drosophila offers many advantages for the detection of mutagenic activity of carcinogenic agents. It provides the quickest assay system for detecting mutations in animals today. Its generation time is short, and Drosophila is cheap and easy to breed in large numbers. The simple genetic testing methods give unequivocal answers about the whole spectrum of relevant genetic damage. A comparison of the detection capacity of assays sampling different kinds of genetic damage revealed that various substances are highly effective in inducing mutations but do not produce chromosome breakage effects at all, or only at much higher concentrations than those required for mutation induction. Of the different assay systems available, the classical sex-linked recessive lethal test deserves priority, in view of its superior capacity to detect mutagens. Of practical importance is also its high sensitivity, because a large number of loci in one fifth of the genome is tested for newly induced forward mutations, including small deletions. The recent findings that Drosophila is capable of carrying out the same metabolic activation reactions as the mammalian liver makes the organism eminently suitable for verifying results obtained in prescreening with fast microbial assay systems. An additional advantage in this respect is the capacity of Drosophila for detecting short-lived activation products, because intracellular metabolic activation appears to occur within the spermatids and spermatocytes.  (+info)

The five amino acid-deleted isoform of hepatocyte growth factor promotes carcinogenesis in transgenic mice. (2/604)

Hepatocyte growth factor (HGF) is a polypeptide with mitogenic, motogenic, and morphogenic effects on different cell types including hepatocytes. HGF is expressed as two biologically active isotypes resulting from alternative RNA splicing. The roles of each HGF isoform in development, liver regeneration and tumorigenesis have not yet been well characterized. We report the generation and analysis of transgenic mice overexpressing the five amino acid-deleted variant of HGF (dHGF) in the liver by virtue of an albumin expression vector. These ALB-dHGF transgenic mice develop normally, have an enhanced rate of liver regeneration after partial hepatectomy, and exhibit a threefold higher incidence of hepatocellular carcinoma (HCC) beyond 17 months of age. Moreover, overexpression of dHGF dramatically accelerates diethyl-nitrosamine induced HCC tumorigenesis. These tumors arise faster, are significantly larger, more numerous and more invasive than those appearing in non-transgenic littermates. Approximately 90% of female dHGF-transgenic mice had multiple macroscopic HCCs 40 weeks after injection of DEN; whereas the non-transgenic counterparts had only microscopic nodules. Liver tumors and cultured tumor cell lines from dHGF transgenics showed high levels of HGF and c-Met mRNA and protein. Together, these results reveal that in vivo dHGF plays an active role in liver regeneration and HCC tumorigenesis.  (+info)

Prokaryotic expression and characterization of human AP DNA endonuclease. (3/604)

The expression of major human apurinic/apyrimidinic DNA endonuclease (APEX) from its cDNA in E. coli (DH5 alpha) was attempted in order to obtain a biologically active recombinant APEX. E. coli cells were transformed by a prokaryotic translation vector (pGEX-4T-3) harboring APEX cDNA. GST-APEX fusion protein with a molecular weight of 6.3 KDa was induced by IPTG (1.0 mM) treatment. Western blot immunodetection identified the induced protein as the GST-APEX fusion protein. The survival rate of E. coli cells (DH5 alpha) transformed with pGEX-4T-3-APEX increased when the cells were treated with N-diethyl-N-nitrosamine (DENA) or 3'-methyl-4-monomethylaminoazobenzene (3'-MeMAB), indicating that APEX expression had a protective effect on the cytotoxicity of these carcinogens. The fusion protein extracted from E. coli cells and purified by GSH-agarose gel affinity chromatography exhibited APEX activity. Treatment of thrombin to the GST-APEX fusion protein and affinity purification followed by Sephacryl S-100 gel filtration resulted in APEX peptide with MW 36 KDa, which exhibited AP DNA repair activity (8,7000 EU/mg protein). N-ethylmaleimide (0.1 mM) or AMP (0.98 mM) inhibited APEX activity by 50% and kinetic analysis indicated that the recombinant APEX (rAPEX) had a Km value of 0.022 microM (AP sites for AP DNA) and the Ki value was 0.48 mM for AMP. These results indicated that E. coli cells expressing biologically active GST-APEX were resistant to the cell damage caused by chemical carcinogens and that rAPEX purified from E. coli cells transformed with APEX cDNA-inserted translation vector was similar to native APEX in some properties.  (+info)

Beta-catenin mutations are frequent in hepatocellular carcinomas but absent in adenomas induced by diethylnitrosamine in B6C3F1 mice. (4/604)

Activating mutations in the region of the beta-catenin gene corresponding to the NH2-terminal phosphorylation sites of glycogen synthetase kinase 3beta have been causally implicated in carcinogenesis. In this study, the beta-catenin exon 3 was examined in hepatic lesions induced by diethylnitrosamine in B6C3F1 mice. PCR and DNA sequencing detected seven beta-catenin mutations in 13 samples dissected from hepatocellular carcinoma tissues, but none in 14 hepatic adenomas. All of the mutations were found in codon 41 encoding a threonine residue, one of the possible glycogen synthetase kinase-3beta phosphorylation sites. Although beta-catenin protein was immunohistochemically stained mainly on the cell membrane in preneoplastic hepatocytic foci and most adenomas, as observed in normal hepatocytes, it was detected in the cytoplasm and nuclei in addition to the cell membrane, indicating stabilization of the protein in HCCs. This shift in staining was observed not only in tumors with mutations, but also in examples lacking exon 3 mutations. Our data demonstrate that beta-catenin alterations may be important for malignant progression during multistep hepatic carcinogenesis in mice.  (+info)

Nordihydroguairetic acid is a potent inhibitor of ferric-nitrilotriacetate-mediated hepatic and renal toxicity, and renal tumour promotion, in mice. (5/604)

Ferric-nitrilotriacetate (Fe-NTA) is a known renal carcinogen. In the present study, we report the effect of a potent lignin-derived herbal antioxidant, nordihydroguairetic acid (NDGA), against Fe-NTA-mediated tissue toxicity. Fe-NTA (alone) treatment of mice enhances ornithine decarboxylase activity to 259% in liver and 341% in kidney and increases [3H]thymidine incorporation in DNA to 250% in liver and 324% in kidney compared with the corresponding saline-treated controls. The enhanced ornithine decarboxylase activity and DNA synthesis showed a reduction to 138 and 123%, respectively, in liver at a higher dose of 2 mg NDGA/day/animal whereas in kidney the reduction was to 118 and 102%, respectively, compared with the corresponding saline-treated controls. In the Fe-NTA (alone)-treated group, a 12% renal tumour incidence was recorded whereas, in N-diethylnitrosamine (DEN)-initiated and Fe-NTA-promoted animals, the percentage tumour incidence was increased to 68% as compared with untreated controls. No tumour incidence was recorded in the DEN-initiated, non-promoted group. The administration of NDGA, afforded >80% protection against DEN- and Fe-NTA-mediated renal tissue injury in vivo. Fe-NTA treatment also enhanced hepatic and renal microsomal lipid peroxidation to 170 and 205% of saline-treated controls, respectively, and hydrogen peroxide generation by >2.5-fold in both tissues accompanied by a 51 and 21% decrease in the level of glutathione and 35-48 and 35-50% decrease in the activities of glutathione-metabolizing and antioxidant enzymes in liver and kidney, respectively. These changes were reversed significantly in animals receiving a pre-treatment of NDGA. Our data show that NDGA can abrogate the toxic and tumour-promoting effects of Fe-NTA in liver and kidney of mice and can serve as a potent chemopreventive agent to suppress oxidant-induced tissue injury and tumorigenesis.  (+info)

Correlation of changes in natural killer cell activity and glutathione S-transferase placental form positive hepatocytes in diethylnitrosamine-induced rat hepatocarcinogenesis. (6/604)

To evaluate the induction of preneoplastic hepatic foci in relation to natural killer cell (NK) activity, we sequentially analyzed glutathione S-transferase placental form positive (GST-P+) hepatocytes and NK activity during diethylnitrosamine (DEN) and phenobarbital (PB)-induced hepatocarcinogenesis in Sprague-Dawley rats. Previous studies have shown that NK activity can modulate the carcinogenic process induced by chemical carcinogens. Newborn females were initially given a single intraperitoneal injection of 15 mg DEN/kg and three weeks later, they were treated with 500 ppm phenobarbital (PB). From week 3, PB was administered in drinking water for 9 weeks. Interim and terminal sacrifices were performed at weeks 12, 15 and 30. GST-P+ hepatocytes increased with age in DEN-treated rats, especially in the population of more than two GST-P+ hepatocytes. The NK activity of DEN-treated rats did not significantly differ from that of control rats until week 12, but it progressively decreased from week 15 to 30. These results indicate that changes of NK activity inversely correlated with the induction of preneoplastic hepatic foci. This strong correlation of decreased NK activity with enhanced induction of GST-P+ foci suggests that NK activity is important in the early progression of hepatocarcinogenesis in rats.  (+info)

Progression of hepatic neoplasia in medaka (Oryzias latipes) exposed to diethylnitrosamine. (7/604)

Progression of hepatic neoplasia was assessed in medaka (Oryzias latipes) following aqueous exposure to diethylnitrosamine (DEN). Larvae (2 weeks old) were exposed to 350 or 500 p.p.m. DEN for 48 h, while adults (3-6 months old) were exposed to 50 p.p.m. DEN for 5 weeks. Fish were maintained as long as possible to determine malignant potential of resultant neoplasms. A total of 423 medaka with 106 hepatic neoplasms were examined. There were marked differences in tumor prevalence between exposure groups including: (i) higher prevalence of hepatocellular carcinomas in medaka exposed as adults (100% of hepatocellular tumors in adult-exposed medaka were malignant, while only 51.5% of larval hepatocellular tumors were malignant); (ii) higher prevalence of biliary tumors in medaka exposed as larvae (46.4% of all tumors in larval-exposed medaka were biliary versus 8.1% in adult-exposed fish); (iii) higher prevalence of mixed hepato-biliary carcinomas in adult-exposed medaka (24.3%) compared with those exposed as larvae (3%). In addition, a unique hepatocellular lesion termed 'nodular proliferation' was only observed in adult-exposed medaka. The lesion was characterized by small size (50-300 microm), complete loss of normal tubular architecture and variable megalocytosis. Nodular proliferation was distinct from preneoplastic foci of cellular alteration and may represent microcarcinomas. There was a step-wise increase in mean diameter with age (days post-exposure) from nodular proliferation (174 microm, 17 days) to hepatocellular carcinoma (1856 microm, 62 days) and mixed carcinomas (3209 microm, 93 days) in adult-exposed medaka. Metastasis was observed with 19 neoplasms and tumors with the highest metastatic potential were hepatocellular and mixed carcinomas. The most common form of metastasis was trans-coelomic, followed by direct invasion and distant metastasis, presumably via the vascular route. Differences in tumor prevalence between exposure groups were believed to be the result of length of DEN exposure rather than age of fish at the time of exposure. In larval medaka with brief (48 h) DEN exposure, neoplasms are thought to be the result of dedifferentiation of hepatic cells, with slow progression of foci of cellular alteration to benign and then malignant tumors. In contrast, with adult medaka and prolonged (5 week) DEN exposure, neoplasms are believed to result from initiation of committed stem cells and formation of microcarcinomas ('nodular proliferation'), before progressing to larger hepatocellular and then mixed carcinomas.  (+info)

The effect of 1/3 partial hepatectomy on the growth of glutathione S-transferase positive foci. (8/604)

Our previous studies indicated that glutathione S-transferase 7-7 (GST 7-7) positive foci induced after initiation have a lower threshold towards proliferative stimuli compared with surrounding hepatocytes. This observation would predict that persistent growth stimuli of low intensity could be very effective in promoting the emergence of focal lesions. To test this possibility, the present study was designed to determine the effect of 1/3 partial hepatectomy (PH) on the incidence and growth of foci in initiated rat liver. The rationale for using a 1/3 PH was that it is known to induce a proliferative response which is less intense but more prolonged compared with that elicited by 2/3 PH. Male Fischer 344 rats (110-120 g) were initiated with diethylnitrosamine (200 mg/kg, i.p.). Three weeks later 1/3 PH (median lobe), 2/3 PH (median and left lobes) or sham operation (SH) was performed. An additional group of initiated animals had the median lobe and the left lobe of the liver removed sequentially (1/3 + 1/3 PH), 3 weeks apart. All rats were killed 8 weeks after carcinogen administration. The results indicated that the number of GST 7-7 positive foci was similar in all groups; however, the percent area occupied by foci was increased in rats receiving 2/3 PH compared with SH (0.21 +/- 0. 08 versus 0.09 +/- 0.03). Interestingly, 1/3 PH was nearly as effective as 2/3 PH in stimulating the growth of foci (percent area 0.18 +/- 0.06 versus 0.21 +/- 0.08), although the magnitude of the stimulus is only half for the former group compared with the latter; peak labeling index was 19 +/- 6 with 1/3 PH compared with 40 +/- 2 with 2/3 PH. Moreover, the maximum increase in the size of foci (percent area 0.37 +/- 0.12) was achieved when the median and left lobes were removed sequentially, three weeks apart. These results indicate that persistent growth stimuli of low intensity can be very effective in promoting the growth of focal lesions.  (+info)

Diethylnitrosamine (DEN) is a potent chemical carcinogen that belongs to the class of nitrosamines. It is known to induce tumors in various organs, including the liver, kidney, and lungs, in different animal species. Diethylnitrosamine requires metabolic activation by enzymes such as cytochrome P450 to exert its carcinogenic effects.

Diethylnitrosamine is not typically used for medical purposes but may be employed in laboratory research to study the mechanisms of chemical carcinogenesis and cancer development. It is essential to handle this compound with care, following appropriate safety protocols, due to its potential hazards.

Experimental liver neoplasms refer to abnormal growths or tumors in the liver that are intentionally created or manipulated in a laboratory setting for the purpose of studying their development, progression, and potential treatment options. These experimental models can be established using various methods such as chemical induction, genetic modification, or transplantation of cancerous cells or tissues. The goal of this research is to advance our understanding of liver cancer biology and develop novel therapies for liver neoplasms in humans. It's important to note that these experiments are conducted under strict ethical guidelines and regulations to minimize harm and ensure the humane treatment of animals involved in such studies.

Nitrosamines are a type of chemical compound that are formed by the reaction between nitrous acid (or any nitrogen oxide) and secondary amines. They are often found in certain types of food, such as cured meats and cheeses, as well as in tobacco products and cosmetics.

Nitrosamines have been classified as probable human carcinogens by the International Agency for Research on Cancer (IARC). Exposure to high levels of nitrosamines has been linked to an increased risk of cancer, particularly in the digestive tract. They can also cause DNA damage and interfere with the normal functioning of cells.

In the medical field, nitrosamines have been a topic of concern due to their potential presence as contaminants in certain medications. For example, some drugs that contain nitrofurantoin, a medication used to treat urinary tract infections, have been found to contain low levels of nitrosamines. While the risk associated with these low levels is not well understood, efforts are underway to minimize the presence of nitrosamines in medications and other products.

2-Acetylaminofluorene (2-AAF) is a chemical compound that has been used in research to study the mechanisms of carcinogenesis. It is an aromatic amine and a derivative of fluorene, with the chemical formula C14H11NO.

2-AAF is not naturally occurring and is synthesized in the laboratory. It has been found to be carcinogenic in animal studies, causing tumors in various organs including the liver, lung, and bladder. The compound is metabolically activated in the body to form reactive intermediates that can bind to DNA and other cellular components, leading to mutations and cancer.

2-AAF has been used as a tool in research to investigate the mechanisms of chemical carcinogenesis and the role of metabolic activation in the process. It is not used in medical treatments or therapies.

Gamma-glutamyltransferase (GGT), also known as gamma-glutamyl transpeptidase, is an enzyme found in many tissues, including the liver, bile ducts, and pancreas. GGT is involved in the metabolism of certain amino acids and plays a role in the detoxification of various substances in the body.

GGT is often measured as a part of a panel of tests used to evaluate liver function. Elevated levels of GGT in the blood may indicate liver disease or injury, bile duct obstruction, or alcohol consumption. However, it's important to note that several other factors can also affect GGT levels, so abnormal results should be interpreted in conjunction with other clinical findings and diagnostic tests.

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.

Phenobarbital is a barbiturate medication that is primarily used for the treatment of seizures and convulsions. It works by suppressing the abnormal electrical activity in the brain that leads to seizures. In addition to its anticonvulsant properties, phenobarbital also has sedative and hypnotic effects, which can be useful for treating anxiety, insomnia, and agitation.

Phenobarbital is available in various forms, including tablets, capsules, and elixirs, and it is typically taken orally. The medication works by binding to specific receptors in the brain called gamma-aminobutyric acid (GABA) receptors, which help to regulate nerve impulses in the brain. By increasing the activity of GABA, phenobarbital can help to reduce excessive neural activity and prevent seizures.

While phenobarbital is an effective medication for treating seizures and other conditions, it can also be habit-forming and carries a risk of dependence and addiction. Long-term use of the medication can lead to tolerance, meaning that higher doses may be needed to achieve the same effects. Abruptly stopping the medication can also lead to withdrawal symptoms, such as anxiety, restlessness, and seizures.

Like all medications, phenobarbital can have side effects, including dizziness, drowsiness, and impaired coordination. It can also interact with other medications, such as certain antidepressants and sedatives, so it is important to inform your healthcare provider of all medications you are taking before starting phenobarbital.

In summary, phenobarbital is a barbiturate medication used primarily for the treatment of seizures and convulsions. It works by binding to GABA receptors in the brain and increasing their activity, which helps to reduce excessive neural activity and prevent seizures. While phenobarbital can be effective, it carries a risk of dependence and addiction and can have side effects and drug interactions.

Alkylating agents are a class of chemotherapy drugs that work by alkylating, or adding an alkyl group to, DNA molecules. This process can damage the DNA and prevent cancer cells from dividing and growing. Alkylating agents are often used to treat various types of cancer, including Hodgkin's lymphoma, non-Hodgkin's lymphoma, multiple myeloma, and solid tumors. Examples of alkylating agents include cyclophosphamide, melphalan, and chlorambucil. These drugs can have significant side effects, including nausea, vomiting, hair loss, and an increased risk of infection. They can also cause long-term damage to the heart, lungs, and reproductive system.

A precancerous condition, also known as a premalignant condition, is a state of abnormal cellular growth and development that has a higher-than-normal potential to progress into cancer. These conditions are characterized by the presence of certain anomalies in the cells, such as dysplasia (abnormal changes in cell shape or size), which can indicate an increased risk for malignant transformation.

It is important to note that not all precancerous conditions will eventually develop into cancer, and some may even regress on their own. However, individuals with precancerous conditions are often at a higher risk of developing cancer compared to the general population. Regular monitoring and appropriate medical interventions, if necessary, can help manage this risk and potentially prevent or detect cancer at an early stage when it is more treatable.

Examples of precancerous conditions include:

1. Dysplasia in the cervix (cervical intraepithelial neoplasia or CIN)
2. Atypical ductal hyperplasia or lobular hyperplasia in the breast
3. Actinic keratosis on the skin
4. Leukoplakia in the mouth
5. Barrett's esophagus in the digestive tract

Regular medical check-ups, screenings, and lifestyle modifications are crucial for individuals with precancerous conditions to monitor their health and reduce the risk of cancer development.

F344 is a strain code used to designate an outbred stock of rats that has been inbreeded for over 100 generations. The F344 rats, also known as Fischer 344 rats, were originally developed at the National Institutes of Health (NIH) and are now widely used in biomedical research due to their consistent and reliable genetic background.

Inbred strains, like the F344, are created by mating genetically identical individuals (siblings or parents and offspring) for many generations until a state of complete homozygosity is reached, meaning that all members of the strain have identical genomes. This genetic uniformity makes inbred strains ideal for use in studies where consistent and reproducible results are important.

F344 rats are known for their longevity, with a median lifespan of around 27-31 months, making them useful for aging research. They also have a relatively low incidence of spontaneous tumors compared to other rat strains. However, they may be more susceptible to certain types of cancer and other diseases due to their inbred status.

It's important to note that while F344 rats are often used as a standard laboratory rat strain, there can still be some genetic variation between individual animals within the same strain, particularly if they come from different suppliers or breeding colonies. Therefore, it's always important to consider the source and history of any animal model when designing experiments and interpreting results.

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.

Cocarcinogenesis is a term used in the field of oncology to describe a process where exposure to certain chemicals or physical agents enhances the tumor-forming ability of a cancer-causing agent (carcinogen). A cocarcinogen does not have the ability to initiate cancer on its own, but it can promote the development and progression of cancer when combined with a carcinogen.

In other words, a cocarcinogen is a substance or factor that acts synergistically with a known carcinogen to increase the likelihood or speed up the development of cancer. This process can occur through various mechanisms, such as suppressing the immune system, promoting inflammation, increasing cell proliferation, or inhibiting apoptosis (programmed cell death).

Examples of cocarcinogens include tobacco smoke, alcohol, certain viruses, and radiation. These agents can interact with carcinogens to increase the risk of cancer in individuals who are exposed to them. It is important to note that while cocarcinogens themselves may not directly cause cancer, they can significantly contribute to its development and progression when combined with other harmful substances or factors.

Liver neoplasms refer to abnormal growths in the liver that can be benign or malignant. Benign liver neoplasms are non-cancerous tumors that do not spread to other parts of the body, while malignant liver neoplasms are cancerous tumors that can invade and destroy surrounding tissue and spread to other organs.

Liver neoplasms can be primary, meaning they originate in the liver, or secondary, meaning they have metastasized (spread) to the liver from another part of the body. Primary liver neoplasms can be further classified into different types based on their cell of origin and behavior, including hepatocellular carcinoma, cholangiocarcinoma, and hepatic hemangioma.

The diagnosis of liver neoplasms typically involves a combination of imaging studies, such as ultrasound, CT scan, or MRI, and biopsy to confirm the type and stage of the tumor. Treatment options depend on the type and extent of the neoplasm and may include surgery, radiation therapy, chemotherapy, or liver transplantation.

Diethylamines are organic compounds that consist of a nitrogen atom bonded to two ethyl groups and one hydrogen atom. The chemical formula for diethylamine is (C2H5)2NH, and it is a colorless liquid with an unpleasant fishy odor. It is used as a building block in the synthesis of various pharmaceuticals, agrochemicals, and other organic compounds. Diethylamines can also be found as byproducts in some industrial processes and are produced naturally by certain plants and animals.

Diethylamines can have stimulant effects on the central nervous system and can cause symptoms such as excitement, restlessness, and confusion. In high concentrations or with prolonged exposure, diethylamines can be toxic and may cause respiratory, cardiovascular, and neurological problems. Therefore, it is important to handle diethylamines with care and use appropriate safety measures when working with them.

Carcinogenicity tests are a type of toxicity test used to determine the potential of a chemical or physical agent to cause cancer. These tests are typically conducted on animals, such as rats or mice, and involve exposing the animals to the agent over a long period of time, often for the majority of their lifespan. The animals are then closely monitored for any signs of tumor development or other indicators of cancer.

The results of carcinogenicity tests can be used by regulatory agencies, such as the U.S. Environmental Protection Agency (EPA) and the Food and Drug Administration (FDA), to help determine safe exposure levels for chemicals and other agents. The tests are also used by industry to assess the potential health risks associated with their products and to develop safer alternatives.

It is important to note that carcinogenicity tests have limitations, including the use of animals, which may not always accurately predict the effects of a chemical on humans. Additionally, these tests can be time-consuming and expensive, which has led to the development of alternative test methods, such as in vitro (test tube) assays and computational models, that aim to provide more efficient and ethical alternatives for carcinogenicity testing.

Heptachlor epoxide is a metabolite and environmental breakdown product of heptachlor, which is a chlorinated hydrocarbon insecticide. It is an organochlorine compound that was widely used in the past for agricultural and residential pest control purposes, including termite treatments and crop protection.

Heptachlor epoxide is formed through the oxidation of heptachlor by various biological and environmental processes. It is more stable and persistent in the environment compared to heptachlor, making it a significant contaminant in soil, water, and air. Heptachlor epoxide has been classified as a probable human carcinogen by the International Agency for Research on Cancer (IARC) and the United States Environmental Protection Agency (EPA). It can accumulate in the fatty tissues of living organisms, including humans, and poses potential risks to human health and the environment.

Glutathione transferases (GSTs) are a group of enzymes involved in the detoxification of xenobiotics and endogenous compounds. They facilitate the conjugation of these compounds with glutathione, a tripeptide consisting of cysteine, glutamic acid, and glycine, which results in more water-soluble products that can be easily excreted from the body.

GSTs play a crucial role in protecting cells against oxidative stress and chemical injury by neutralizing reactive electrophilic species and peroxides. They are found in various tissues, including the liver, kidneys, lungs, and intestines, and are classified into several families based on their structure and function.

Abnormalities in GST activity have been associated with increased susceptibility to certain diseases, such as cancer, neurological disorders, and respiratory diseases. Therefore, GSTs have become a subject of interest in toxicology, pharmacology, and clinical research.

Hepatectomy is a surgical procedure that involves the removal of part or all of the liver. This procedure can be performed for various reasons, such as removing cancerous or non-cancerous tumors, treating liver trauma, or donating a portion of the liver to another person in need of a transplant (live donor hepatectomy). The extent of the hepatectomy depends on the medical condition and overall health of the patient. It is a complex procedure that requires significant expertise and experience from the surgical team due to the liver's unique anatomy, blood supply, and regenerative capabilities.

Dimethylnitrosamine is a chemical compound with the formula (CH3)2NNO. It is a potent carcinogen, and is classified as a Class 1 carcinogen by the International Agency for Research on Cancer (IARC). It is known to cause cancer in various organs, including the liver, kidney, and lungs.

Dimethylnitrosamine is formed when nitrogen oxides react with secondary amines under conditions that are commonly encountered in industrial processes or in certain food preservation methods. It can also be found as a contaminant in some foods and cosmetics.

Exposure to dimethylnitrosamine can occur through inhalation, ingestion, or skin contact. The toxic effects of this compound are due to its ability to form DNA adducts, which can lead to mutations and cancer. It is important to minimize exposure to this compound and to take appropriate safety measures when working with it.

A liver cell adenoma is a benign tumor that develops in the liver and is composed of cells similar to those normally found in the liver (hepatocytes). These tumors are usually solitary, but multiple adenomas can occur, especially in women who have taken oral contraceptives for many years. Liver cell adenomas are typically asymptomatic and are often discovered incidentally during imaging studies performed for other reasons. In rare cases, they may cause symptoms such as abdominal pain or discomfort, or complications such as bleeding or rupture. Treatment options include monitoring with periodic imaging studies or surgical removal of the tumor.

Hepatocellular carcinoma (HCC) is the most common type of primary liver cancer in adults. It originates from the hepatocytes, which are the main functional cells of the liver. This type of cancer is often associated with chronic liver diseases such as cirrhosis caused by hepatitis B or C virus infection, alcohol abuse, non-alcoholic fatty liver disease (NAFLD), and aflatoxin exposure.

The symptoms of HCC can vary but may include unexplained weight loss, lack of appetite, abdominal pain or swelling, jaundice, and fatigue. The diagnosis of HCC typically involves imaging tests such as ultrasound, CT scan, or MRI, as well as blood tests to measure alpha-fetoprotein (AFP) levels. Treatment options for Hepatocellular carcinoma depend on the stage and extent of the cancer, as well as the patient's overall health and liver function. Treatment options may include surgery, radiation therapy, chemotherapy, targeted therapy, or liver transplantation.

Organ size refers to the volume or physical measurement of an organ in the body of an individual. It can be described in terms of length, width, and height or by using specialized techniques such as imaging studies (like CT scans or MRIs) to determine the volume. The size of an organ can vary depending on factors such as age, sex, body size, and overall health status. Changes in organ size may indicate various medical conditions, including growths, inflammation, or atrophy.

"Oryzias" is not a medical term, but a genus name in the family Adrianichthyidae, which includes various species of small fish commonly known as "ricefishes" or "medaka." These fish are often used in scientific research, particularly in the fields of genetics and developmental biology. They are not associated with human diseases or medical conditions.

Pentachlorophenol is not primarily a medical term, but rather a chemical compound with some uses and applications in the medical field. Medically, it's important to understand what pentachlorophenol is due to its potential health implications.

Pentachlorophenol (PCP) is an organochlorine compound that has been widely used as a pesticide, wood preservative, and disinfectant. Its chemical formula is C6HCl5O. It is a white crystalline solid with a distinct, somewhat unpleasant odor. In the environment, pentachlorophenol can be found in soil, water, and air as well as in various organisms, including humans.

Pentachlorophenol has been associated with several potential health risks. It is classified as a probable human carcinogen by the International Agency for Research on Cancer (IARC) and as a possible human carcinogen by the United States Environmental Protection Agency (EPA). Exposure to pentachlorophenol can occur through inhalation, skin contact, or ingestion. Potential health effects include irritation of the skin, eyes, and respiratory tract; damage to the liver and kidneys; neurological issues; and reproductive problems.

In a medical context, pentachlorophenol might be relevant in cases where individuals have been exposed to this compound through occupational or environmental sources. Medical professionals may need to assess potential health risks, diagnose related health issues, and provide appropriate treatment.

Experimental neoplasms refer to abnormal growths or tumors that are induced and studied in a controlled laboratory setting, typically in animals or cell cultures. These studies are conducted to understand the fundamental mechanisms of cancer development, progression, and potential treatment strategies. By manipulating various factors such as genetic mutations, environmental exposures, and pharmacological interventions, researchers can gain valuable insights into the complex processes underlying neoplasm formation and identify novel targets for cancer therapy. It is important to note that experimental neoplasms may not always accurately represent human cancers, and further research is needed to translate these findings into clinically relevant applications.

Choline deficiency is a condition that occurs when an individual's diet does not provide adequate amounts of choline, which is an essential nutrient required for various bodily functions. Choline plays a crucial role in the synthesis of phospholipids, which are critical components of cell membranes, and it also serves as a precursor to the neurotransmitter acetylcholine, which is involved in memory, muscle control, and other nervous system functions.

Choline deficiency can lead to several health problems, including fatty liver disease, muscle damage, and cognitive impairment. Symptoms of choline deficiency may include fatigue, memory loss, cognitive decline, and peripheral neuropathy. In severe cases, it can also cause liver dysfunction and even liver failure.

It is important to note that choline deficiency is relatively rare in the general population, as many foods contain choline, including eggs, meat, fish, dairy products, and certain vegetables such as broccoli and Brussels sprouts. However, some individuals may be at higher risk of choline deficiency, including pregnant women, postmenopausal women, and those with certain genetic mutations that affect choline metabolism. In these cases, supplementation with choline may be necessary to prevent deficiency.

Methyldimethylaminoazobenzene is not typically referred to in a medical context, but it is a chemical compound that has been used in research and industry. It's a type of azo dye with the molecular formula C12H15N3O.

In a medical or toxicological context, this compound might be mentioned due to its potential harmful effects. It is known to be carcinogenic (cancer-causing) and mutagenic (DNA-damaging) in experimental animals, and exposure to it has been associated with an increased risk of liver cancer in humans. However, it's important to note that this compound is not used in medicine or medical research and its use is generally discouraged due to its harmful effects.

Glucose-6-phosphatase is an enzyme that plays a crucial role in the regulation of glucose metabolism. It is primarily located in the endoplasmic reticulum of cells in liver, kidney, and intestinal mucosa. The main function of this enzyme is to remove the phosphate group from glucose-6-phosphate (G6P), converting it into free glucose, which can then be released into the bloodstream and used as a source of energy by cells throughout the body.

The reaction catalyzed by glucose-6-phosphatase is as follows:

Glucose-6-phosphate + H2O → Glucose + Pi (inorganic phosphate)

This enzyme is essential for maintaining normal blood glucose levels, particularly during periods of fasting or starvation. In these situations, the body needs to break down stored glycogen in the liver and convert it into glucose to supply energy to the brain and other vital organs. Glucose-6-phosphatase is a key enzyme in this process, allowing for the release of free glucose into the bloodstream.

Deficiencies or mutations in the gene encoding glucose-6-phosphatase can lead to several metabolic disorders, such as glycogen storage disease type I (von Gierke's disease) and other related conditions. These disorders are characterized by an accumulation of glycogen and/or fat in various organs, leading to impaired glucose metabolism, growth retardation, and increased risk of infection and liver dysfunction.

Alkylation, in the context of medical chemistry and toxicology, refers to the process of introducing an alkyl group (a chemical moiety made up of a carbon atom bonded to one or more hydrogen atoms) into a molecule, typically a biomolecule such as a protein or DNA. This process can occur through various mechanisms, including chemical reactions with alkylating agents.

In the context of cancer therapy, alkylation is used to describe a class of chemotherapeutic drugs known as alkylating agents, which work by introducing alkyl groups onto DNA molecules in rapidly dividing cells. This can lead to cross-linking of DNA strands and other forms of DNA damage, ultimately inhibiting cell division and leading to the death of cancer cells. However, these agents can also affect normal cells, leading to side effects such as nausea, hair loss, and increased risk of infection.

It's worth noting that alkylation can also occur through non-chemical means, such as in certain types of radiation therapy where high-energy particles can transfer energy to electrons in biological molecules, leading to the formation of reactive radicals that can react with and alkylate DNA.

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.

Methylcholanthrene is a polycyclic aromatic hydrocarbon that is used in research to induce skin tumors in mice. It is a potent carcinogen and mutagen, and exposure to it can increase the risk of cancer in humans. It is not typically found in medical treatments or therapies.

Anticarcinogenic agents are substances that prevent, inhibit or reduce the development of cancer. They can be natural or synthetic compounds that interfere with the process of carcinogenesis at various stages, such as initiation, promotion, and progression. Anticarcinogenic agents may work by preventing DNA damage, promoting DNA repair, reducing inflammation, inhibiting cell proliferation, inducing apoptosis (programmed cell death), or modulating immune responses.

Examples of anticarcinogenic agents include chemopreventive agents, such as nonsteroidal anti-inflammatory drugs (NSAIDs) and retinoids; phytochemicals found in fruits, vegetables, and other plant-based foods; and medications used to treat cancer, such as chemotherapy, radiation therapy, and targeted therapies.

It is important to note that while some anticarcinogenic agents have been shown to be effective in preventing or reducing the risk of certain types of cancer, they may also have potential side effects and risks. Therefore, it is essential to consult with a healthcare professional before using any anticarcinogenic agent for cancer prevention or treatment purposes.

Hepatocytes are the predominant type of cells in the liver, accounting for about 80% of its cytoplasmic mass. They play a key role in protein synthesis, protein storage, transformation of carbohydrates, synthesis of cholesterol, bile salts and phospholipids, detoxification, modification, and excretion of exogenous and endogenous substances, initiation of formation and secretion of bile, and enzyme production. Hepatocytes are essential for the maintenance of homeostasis in the body.

Methylnitrosourea (MNU) is not a medical term per se, but it is a chemical compound that has been widely used in biomedical research, particularly in cancer studies. Therefore, I will provide you with a scientific definition of this compound.

Methylnitrosourea (MNU) is an alkylating agent and a nitrosourea compound. It is known to be highly mutagenic and carcinogenic. MNU acts by transferring its methyl group (-CH3) to DNA, RNA, and proteins, causing damage to these macromolecules. This methylation can lead to point mutations, chromosomal aberrations, and DNA strand breaks, which contribute to genomic instability and cancer initiation and progression.

In research settings, MNU has been used as a model carcinogen to induce tumors in various animal models, primarily rodents, to study the mechanisms of carcinogenesis and evaluate potential chemopreventive or therapeutic agents. However, due to its high toxicity and mutagenicity, handling and use of MNU require strict safety measures and precautions.

Body weight is the measure of the force exerted on a scale or balance by an object's mass, most commonly expressed in units such as pounds (lb) or kilograms (kg). In the context of medical definitions, body weight typically refers to an individual's total weight, which includes their skeletal muscle, fat, organs, and bodily fluids.

Healthcare professionals often use body weight as a basic indicator of overall health status, as it can provide insights into various aspects of a person's health, such as nutritional status, metabolic function, and risk factors for certain diseases. For example, being significantly underweight or overweight can increase the risk of developing conditions like malnutrition, diabetes, heart disease, and certain types of cancer.

It is important to note that body weight alone may not provide a complete picture of an individual's health, as it does not account for factors such as muscle mass, bone density, or body composition. Therefore, healthcare professionals often use additional measures, such as body mass index (BMI), waist circumference, and blood tests, to assess overall health status more comprehensively.

Histochemistry is the branch of pathology that deals with the microscopic localization of cellular or tissue components using specific chemical reactions. It involves the application of chemical techniques to identify and locate specific biomolecules within tissues, cells, and subcellular structures. This is achieved through the use of various staining methods that react with specific antigens or enzymes in the sample, allowing for their visualization under a microscope. Histochemistry is widely used in diagnostic pathology to identify different types of tissues, cells, and structures, as well as in research to study cellular and molecular processes in health and disease.

Clofibrate is a medication that belongs to the class of drugs known as fibrates. It is primarily used to lower elevated levels of cholesterol and other fats (lipids) in the blood, specifically low-density lipoprotein (LDL), or "bad" cholesterol, and triglycerides, while increasing high-density lipoprotein (HDL), or "good" cholesterol. Clofibrate works by reducing the production of very-low-density lipoproteins (VLDL) in the liver, which in turn lowers triglyceride levels and indirectly reduces LDL cholesterol levels.

Clofibrate is available in oral tablet form and is typically prescribed for patients with high cholesterol or triglycerides who are at risk of cardiovascular disease, such as those with a history of heart attacks, strokes, or peripheral artery disease. It is important to note that clofibrate should be used in conjunction with lifestyle modifications, including a healthy diet, regular exercise, and smoking cessation.

Like all medications, clofibrate can have side effects, some of which may be serious. Common side effects include stomach upset, diarrhea, gas, and changes in taste. Less commonly, clofibrate can cause more severe side effects such as liver or muscle damage, gallstones, and an increased risk of developing certain types of cancer. Patients taking clofibrate should be monitored regularly by their healthcare provider to ensure that the medication is working effectively and to monitor for any potential side effects.

"Inbred strains of rats" are genetically identical rodents that have been produced through many generations of brother-sister mating. This results in a high degree of homozygosity, where the genes at any particular locus in the genome are identical in all members of the strain.

Inbred strains of rats are widely used in biomedical research because they provide a consistent and reproducible genetic background for studying various biological phenomena, including the effects of drugs, environmental factors, and genetic mutations on health and disease. Additionally, inbred strains can be used to create genetically modified models of human diseases by introducing specific mutations into their genomes.

Some commonly used inbred strains of rats include the Wistar Kyoto (WKY), Sprague-Dawley (SD), and Fischer 344 (F344) rat strains. Each strain has its own unique genetic characteristics, making them suitable for different types of research.

Deoxyguanosine is a chemical compound that is a component of DNA (deoxyribonucleic acid), one of the nucleic acids. It is a nucleoside, which is a molecule consisting of a sugar (in this case, deoxyribose) and a nitrogenous base (in this case, guanine). Deoxyguanosine plays a crucial role in the structure and function of DNA, as it pairs with deoxycytidine through hydrogen bonding to form a rung in the DNA double helix. It is involved in the storage and transmission of genetic information.

Neoplastic cell transformation is a process in which a normal cell undergoes genetic alterations that cause it to become cancerous or malignant. This process involves changes in the cell's DNA that result in uncontrolled cell growth and division, loss of contact inhibition, and the ability to invade surrounding tissues and metastasize (spread) to other parts of the body.

Neoplastic transformation can occur as a result of various factors, including genetic mutations, exposure to carcinogens, viral infections, chronic inflammation, and aging. These changes can lead to the activation of oncogenes or the inactivation of tumor suppressor genes, which regulate cell growth and division.

The transformation of normal cells into cancerous cells is a complex and multi-step process that involves multiple genetic and epigenetic alterations. It is characterized by several hallmarks, including sustained proliferative signaling, evasion of growth suppressors, resistance to cell death, enabling replicative immortality, induction of angiogenesis, activation of invasion and metastasis, reprogramming of energy metabolism, and evading immune destruction.

Neoplastic cell transformation is a fundamental concept in cancer biology and is critical for understanding the molecular mechanisms underlying cancer development and progression. It also has important implications for cancer diagnosis, prognosis, and treatment, as identifying the specific genetic alterations that underlie neoplastic transformation can help guide targeted therapies and personalized medicine approaches.

Hyperplasia is a medical term that refers to an abnormal increase in the number of cells in an organ or tissue, leading to an enlargement of the affected area. It's a response to various stimuli such as hormones, chronic irritation, or inflammation. Hyperplasia can be physiological, like the growth of breast tissue during pregnancy, or pathological, like in the case of benign or malignant tumors. The process is generally reversible if the stimulus is removed. It's important to note that hyperplasia itself is not cancerous, but some forms of hyperplasia can increase the risk of developing cancer over time.

"Mesocricetus" is a genus of rodents, more commonly known as hamsters. It includes several species of hamsters that are native to various parts of Europe and Asia. The best-known member of this genus is the Syrian hamster, also known as the golden hamster or Mesocricetus auratus, which is a popular pet due to its small size and relatively easy care. These hamsters are burrowing animals and are typically solitary in the wild.

"Wistar rats" are a strain of albino rats that are widely used in laboratory research. They were developed at the Wistar Institute in Philadelphia, USA, and were first introduced in 1906. Wistar rats are outbred, which means that they are genetically diverse and do not have a fixed set of genetic characteristics like inbred strains.

Wistar rats are commonly used as animal models in biomedical research because of their size, ease of handling, and relatively low cost. They are used in a wide range of research areas, including toxicology, pharmacology, nutrition, cancer, cardiovascular disease, and behavioral studies. Wistar rats are also used in safety testing of drugs, medical devices, and other products.

Wistar rats are typically larger than many other rat strains, with males weighing between 500-700 grams and females weighing between 250-350 grams. They have a lifespan of approximately 2-3 years. Wistar rats are also known for their docile and friendly nature, making them easy to handle and work with in the laboratory setting.

  • Resveratrol suppresses oxidative stress and inflammatory response in diethylnitrosamine-initiated rat hepatocarcinogenesis. (greenmedinfo.com)
  • 2002 ▶ ). It has been reported that TQ supplementation prevents the development of diethylnitrosamine-induced initiation of liver cancer in rats by decreasing oxidative stress biomarkers such as NO (Sayed-Ahmed et al. (weeksmd.com)
  • In this study, we investigated the molecular mechanism of the inhibitory effects of dietary supplementation with AUR on N,N-diethylnitrosamine (DEN)-initiated hepatocarcinogenesis. (nih.gov)
  • Kinetics of Diethylnitrosamine Hepatocarcinogenesis in the Infant Mouse. (aacrjournals.org)
  • Diethylnitrosamine is well known for its toxic and carcinogenic properties affecting mainly liver and kidneys. (vfu.cz)
  • In this study we used diethylnitrosamine induced mouse experimental model of liver and kidney damage to assess the potential chemopreventive effect of capsaicin in vivo . (vfu.cz)
  • Histological evaluation of the liver and kidneys revealed toxic damage of diethylnitrosamine treated animals, whereas mice that received the combination of the substances showed milder lesions. (vfu.cz)
  • Proliferating cell nuclear antigen expression was lower in diethylnitrosamine treated animals compared to the control and capsaicin groups, pointing to a disruption of the proliferative activity of hepatocytes in the juvenile liver. (vfu.cz)
  • In conclusion, our experiment demonstrated the toxic properties of diethylnitrosamine in mice liver and kidneys, with the promising beneficial effect of capsaicin. (vfu.cz)
  • Peroxisome proliferator-activated receptor γ ligands suppress liver carcinogenesis induced by diethylnitrosamine in rats. (wjgnet.com)
  • Furthermore, we found that part of hepatocyte express SOX9 during formation of hepatocellular carcinoma induced by diethylnitrosamine. (nii.ac.jp)
  • paniala seeds attenuated the early stage of diethylnitrosamine and 1,2-dimethylhydrazine-induced colorectal carcinogenesis. (bvsalud.org)
  • Background: Diethylnitrosamine (DENA), a well-known dietary carcinogen, related to cancer initiation of various<br />organs. (waocp.org)
  • Quantitative Image Cytometry of Hepatocytes Expressing Gamma-Glutamyl Transpeptidase and Glutathione S-Transferase in Diethylnitrosamine-Initiated Rats Treated with Phenobarbitol and/or Phthalate Esters. (epa.gov)
  • By using the modified Ito medium-term bioassay protocol, male F344 rats were given a single ip dose of 200 mg/kg of diethylnitrosamine (DEN) as an initiator. (cdc.gov)
  • The system is fundamentally based on the two-stage hypothesis of oarcinogenesis : intiation with diethylnitrosamine (200 mg/kg bw, ip) is follwed by test chemical administration during the second, in combination with 2/3 partial hepatectomy. (go.jp)
  • 14. Suppressive effects of thymoquinone on the initiation stage of diethylnitrosamine hepatocarcinogenesis in rats. (nih.gov)
  • 3. Standardization of diethylnitrosamine-induced hepatocellular carcinoma rat model with time based molecular assessment. (nih.gov)
  • 6. Anti-cancer effects of Ajwa dates (Phoenix dactylifera L.) in diethylnitrosamine induced hepatocellular carcinoma in Wistar rats. (nih.gov)
  • 10. Effect of two selenium sources on hepatocarcinogenesis and several angiogenic cytokines in diethylnitrosamine-induced hepatocarcinoma rats. (nih.gov)
  • 12. Piperlongumine inhibits diethylnitrosamine induced hepatocellular carcinoma in rats. (nih.gov)
  • 13. Involvement of NF-κB/PI3K/AKT signaling pathway in the protective effect of prunetin against a diethylnitrosamine induced hepatocellular carcinogenesis in rats. (nih.gov)
  • 15. Protective effects of Celastrol on diethylnitrosamine-induced hepatocellular carcinoma in rats and its mechanisms. (nih.gov)
  • 18. Chemopreventive and Therapeutic Efficacy of Enhalus acoroides against Diethylnitrosamine Induced Hepatocellular Carcinoma in Wistar Albino Rats. (nih.gov)
  • By using the modified Ito medium-term bioassay protocol, male F344 rats were given a single ip dose of 200 mg/kg of diethylnitrosamine (DEN) as an initiator. (cdc.gov)
  • Ursolic acid attenuates oxidative stress-mediated hepatocellular carcinoma induction by diethylnitrosamine in male Wistar rats. (herbshealthhappiness.com)
  • In this research, a homeopathic model was employed to detect - through the behavior of lab rats during the period of 30 days of the experiment, as well as through hepatic cytology and histology - the influence of ultradilutions 30 CH of Dexamethazon, Diethylnitrosamine (DEN) and Acetylaminofluorene (AAF) applied in animals with previously induced carcinogenesis by the carcinogenic drugs Diethylnitrosamine and Acetylaminofluorene. (unesp.br)
  • Behavioural and brain tissue-associated biochemical changes on LPS challenge have been assayed in a Diethylnitrosamine (DEN)-treated Wistar rat model of hepatic cancer. (ijpsr.com)
  • Highly susceptible to the induction of liver tumours by N,N-diethylnitrosamine. (jax.org)
  • Molecular Changes Following Induction of Hepatocellular Carcinoma by Diethylnitrosamine and Thioacetamide, and Subsequent Treatment with Dioscorea membranacea Extract. (nih.gov)
  • Ces patientes ont été soumises à une induction d'ovulation et ont reçu, sur la base d'une répartition aléatoire et en aveugle, de la silymarine (70 mg × 3 fois par jour) ou un placebo, dès le début du cycle d'induction. (who.int)
  • Diethylnitrosamine was used to induce liver cancer in a rat model. (nih.gov)
  • 19. Safety and Feasibility of Contrast-Enhanced Computed Tomography with a Nanoparticle Contrast Agent for Evaluation of Diethylnitrosamine-Induced Liver Tumors in a Rat Model. (nih.gov)
  • We also detected the high expression pattern of GAS2L3 , SEMA3F , SNRPA , and SNRPD2 in the datasets of GSE102079, GSE76427, GSE64041, GSE121248, GSE84005, and the qPCR assay using diethylnitrosamine-induced HCC mouse model. (biomedcentral.com)
  • objectives: the current study aimed to investigate the hepatic and renal protective effects of aerial parts of echinacea purpurea extract (epe) on injury induced by diethylnitrosamine (den). (gov.ir)
  • 8. Hepatic inflammation-fibrosis-cancer axis in the rat hepatocellular carcinoma induced by diethylnitrosamine. (nih.gov)
  • We will treat mice (male and female) with a single injection of a hepatic carcinogen, diethylnitrosamine (DEN), followed by continued exposure to HRCD with or without BCX (or SRPE) intervention. (usda.gov)
  • Diethylnitrosamine (DEN) of 15 mg/kg body weight was injected to newborn Sprague-Dawley rat subcutaneously within 24 hours, and after 3 weeks, Chinese cabbage (95% ethanol extract) was given at a dose of 2 mg/ml in drinking water. (e-crt.org)
  • Preneoplastic and neoplastic progression during hepatocarcinogenesis in mice injected with diethylnitrosamine in infancy. (nih.gov)
  • 9. Maotai ameliorates diethylnitrosamine-initiated hepatocellular carcinoma formation in mice. (nih.gov)
  • We found that the expression of vasa is induced in the gut and regenerating fin by exposure to a carcinogen, diethylnitrosamine (DEN). (elsevierpure.com)
  • 1. Dietary modulations of folic acid affect the development of diethylnitrosamine induced hepatocellular carcinoma in a rat model. (nih.gov)
  • 4. Attenuation of diethylnitrosamine-induced hepatocellular carcinoma in a rat model by combination therapy of diacerein and gold nanoparticles: a histopathological and immunohistochemical study. (nih.gov)
  • The expression patterns of several targeting genes were also verified by analyzing the Chinese HLivH060PG02 HCC cohort, several GEO datasets, HPA database, and diethylnitrosamine-induced HCC mouse model. (biomedcentral.com)
  • Furthermore, we confirmed the expression feature and prognostic value of several novel targeting genes, using our Chinese HLivH060PG02 HCC cohort, the Diethylnitrosamine-induced HCC mouse model, the available datasets of TCGA, GEO, and HPA database, respectively. (biomedcentral.com)
  • Glandular/acinar formation in a diethylnitrosamine-induced hepatocellular adenoma. (nih.gov)
  • Previously we showed that inappropriate expression and chronic activity of FGF receptor (FGFR) 1 in hepatocytes accelerated diethylnitrosamine (DEN)-initiated hepatocarcinogenesis. (elsevierpure.com)

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