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Cadmium Poisoning definition: Poisoning occurring after exposure to cadmium compounds or fumes. It may cause gastrointestinal syndromes, anemia, or pneumonitis.
Drug Toxicity definition: Manifestations of the adverse effects of drugs administered therapeutically or in the course of diagnostic techniques. It does not include accidental or intentional poisoning for which specific headings are available.
Drug Toxicity definition: An adverse effect of a drug used therapeutically or diagnostically.
Mushroom Poisoning definition: Poisoning from ingestion of mushrooms, primarily from, but not restricted to, toxic varieties.
Mutagenicity Tests definition: Tests of chemical substances and physical agents for mutagenic potential. They include microbial, insect, mammalian cell, and whole animal tests.
mutagen testing definition: tests of chemical substances and physical agents for mutagenic potential, including cell culture, microbial, insect, mammalian cell, and whole animal tests.
toxicity definition: Used with drugs and chemicals for experimental human and animal studies of their ill effects. It includes studies to determine the margin of safety or the reactions accompanying administration at various dose levels. It is used also for exposure to environmental agents. Poisoning should be considered for life-threatening exposure to environmental agents.
neurotoxicity definition: The tendency of some treatments to cause damage to the nervous system.
Neurotoxicity Syndromes definition: Neurologic disorders caused by exposure to toxic substances through ingestion, injection, cutaneous application, or other method. This includes conditions caused by biologic, chemical, and pharmaceutical agents.
Toxicity Tests definition: An array of tests used to determine the toxicity of a substance to living systems. These include tests on clinical drugs, foods, and environmental pollutants.
Toxicity Test definition: Controlled laboratory tests to determine the toxicity of a chemical to an organism in terms of specific chemical concentrations.
carbon tetrachloride poisoning definition: inhalation of vapors, ingestion, or skin absorption of carbon tetrachloride can depress central nervous system activity and cause degeneration of the liver and kidneys.
Toxicity definition: The finding of bodily harm due to the poisonous effects of something.
cardiotoxicity definition: Toxicity that affects the heart.
Cardiotoxicity definition: Toxicity that impairs or damages the heart. This condition is often caused by the administration of a pharmaceutical agent that initiates a poisonous or toxic response in cardiac tissue.
irreversible toxicity definition: Side effects that are caused by toxic substances or something harmful to the body and do not go away.
Acute Toxicity Tests definition: Experiments designed to determine the potential toxic effects of one-time, short-term exposure to a chemical or chemicals.
Mitochondrial Damage definition: Mitochondrial Damage involves any process that leads to dysfunction of mitochondria, whether by oxidative damage, mutation of mitochondrial DNA or other by means.
Toxicity Tests, Chronic definition: Experiments designed to determine the potential toxic effects of a long-term exposure to a chemical or chemicals.
FADD Gene definition: This gene is involved in signal transduction and the activation of caspase-dependent apoptosis.
Acetaminophen Pathway definition: Acetaminophen is one of the world's most commonly used drugs, used for the treatment of pain and fever. Like other NSAIDs (non-steroidal anti-inflammatory drugs), acetaminophen has a unique activity profile based in part on its action at its molecular targets, the cyclooxygenase enzymes that produce prostaglandins responsible for pain, fever and inflammation. Until very recently, only two Cox enzymes, Cox-1 and Cox-2, were known to be targets of NSAIDS. Cox-1 is expressed in a constitutive manner throughout most tissues, and plays an essential role in maintaining the integrity of the stomach mucosal lining. Cox-2 is an inducible enzyme whose expression is induced by inflammation. NSAIDS selective for Cox-2 have been developed to avoid the development of ulcers by some non-selective NSAIDs, including aspirin. While these two isoforms were sufficient to account for most NSAIDs pharmacology, the actions of acetaminophen remained hard to explain on the basis of inhibiting Cox-1 and Cox-2 alone, such as its efficacy at reducing pain and fever but lack of anti-inflammatory effects. A novel Cox enzyme isoform encoded by the Cox-1 gene, Cox-3, contains an additional 30-34 amino acids and is expressed selectively in the brain. This insertion alters the pharmacology of the Cox enzyme, making Cox-3 sensitive to selective inhibition by acetaminophen and other drugs that reduce pain and fever but have weak anti-inflammatory activity, explaining the pharmacology of these drugs. Another characteristic of acetaminophen is its liver toxicity when taken at high doses. The target of this toxicity has also been recently been revealed. The nuclear receptor CAR is activated by many different exogenous compounds, including acetaminophen, inducing expression of three cytochrome P450 enzymes that transform acetaminophen into NAPQI, a reactive and toxic metabolite. Blocking CAR activation with an antagonist protects against acetaminophen liver toxicity, suggesting a strategy to treat acetaminophen toxicity. (BioCarta)
Common Terminology Criteria for Adverse Events definition: A standard terminology developed to report adverse events occurring in cancer clinical trials. Common terminology criteria for adverse events (CTCAE) are used in study adverse event summaries and Investigational New Drug reports to the Food and Drug Administration. The CTCAE contain a grading scale for each adverse event term representing the severity of the event.
Lipid Metabolism and Toxicity Pathway definition: Nuclear receptors are transcription factors that are activated upon binding to its ligands. Initially, they had been classified as classic endocrine nuclear hormone receptors and orphan receptors. However, further studies have led to the identification of lipid ligands for some of these receptors, which are responsible for lipid metabolism, storage, and elimination. One of the characteristics of these receptors is that they act by forming heterodimers with retinoid X receptor (RXR). The receptors include peroxisome proliferators-Activated receptors (PPARs) for fatty acids, liver X receptor (LCR) for oxysterols, Farnesoid X receptors (FXR) for bile acids, and steroid xenobiotic receptor/X receptor (SXR/PXR or Nsil2) for xenobiotics. Other orphan receptors also requiring RXR for its functions are vitamin D receptor (VDR) for vitamin D and retinoic acid receptor (RAR) for retinoid acids, although these receptors are not involved in lipid metabolism. Upon binding to various ligands, three classes of proteins are synthesized including lipid binding proteins, the ATP-binding cassette (ABC) transporters and cytochrome P450 member proteins which catalyze lipid anabolism, metabolism, and elimination. In addition to lipid metabolism, some members of the cytochrome P450 family genes are responsible for activation of procarcinogens, detoxification of environmental toxins, and metabolism of drugs and xenobiotics. In particular, CAR, Nsil2, and recently identified VDR are important in up-regulation of these cytochromes. Of all the human cytochrome P450 genes, only a few CYP1A2, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A4 account for most toxicity effects, specifically CYP3A is responsible for clearing approximately half of the clinically prescribed drugs. For instance, acetaminophen, one of the most commonly used drug, is toxic in high doses due to the activation of CAR and the drug's subsequent conversion to acetyl-p-benzoquinone imine (NAPQI) by CYP1A2, CYP2E1 and CYP3A. (BioCarta)
Adverse Event Toxicity Grade definition: The toxicity grade value of the adverse event.
toxicité definition: Capacité d’une substance à provoquer un effet néfaste voir létal pour un être humain, une bactérie ou une plante.