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ClassyFire Ontology
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| CATEGORY | QUALITY | THRESHOLD | OCCURENCE | REFERENCE |
|---|---|---|---|---|
| smell | woodruff-like | 7.527e-2 µmol/L | raw licorice | details |
| smell | woodruff-like | 7.527e-2 µmol/L | licorice | details |
| smell | woodruff-like | 7.527e-2 µmol/L | green tea | details |
| Toxicity Summary |
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| Link to the Distributed Structure-Searchable Toxicity (DSSTox) Database |
| IDENTIFICATION: Coumarin occurs in fruits, roots, bark, stalks, leaves and branches of a wide variety of plants including Tonka bean, cassie, levender, lovage, yellow sweet clover, deer tongue and woodruff. It is used as a flavoring agent in food; a fixative and enhancer for the odor of essential oils in perfumes; in toilet soaps, toothpastes and in hair preparations; in tobacco products to enhance and fix the natural taste, flavor and aroma; and in industrial products to mask disagreeable odors. HUMAN EXPOSURE: Four male and four female volunteers were given 200 mg each of coumarin in a capsule. Most of dose was excreted in the first 24 hr, primarily as 7-hydroxycoumarin and another metabolic product O-hydroxyphenylacetic acid. Blood concentration time profiles calculated after oral or iv administration of coumarin to four male and two female adults indicated an open two compartment model. The major site of metabolism is the liver and the glucuronidation of the metabolites may occur at several sites, including the liver and intestinal wall along with other tissues. ANIMAL STUDIES: Coumarin administered to female Albino rats caused hyperglycemia which lasted about 24 hr. An oral dose of coumarin dissolved in Arachis oil administered daily for seven dats to virgin female Wistar rats resulted in a decrease in serum progesterone levels. Groups of six male rats were given coumarin in Arachis oil daily for seven days by oral intubation. There was no increase in relative liver weight at lower doses; however, there was a dose related increase at the highest dose tested. Histological changes at the highest dose consisted of fatty change abd vacuolar degeneration in the centrilobular hepatocytes. A centrilobular loss of G6P and aniline hydroxylase resulted at the two highest doses. Lysosomal and ultrastructural changes also occurred at the two highest doses; the latter consisted of hypertrophy and dilation of the rough endoplasmic reticulium in centrilobular hepatocytes, increases in the size of lysosomes and the number of autophagic vacoules. Dose related depression in cytochrome p-450 and aminopyridine demethylase also occurred at the two highest dose levels. Coumarin was fed for 32 weeks in the diet to DBA/2 mice and to CH3/HeJ mice. Minimal increases in serum glutamate oxalate transferase, gamma-glutamyl transferase and sorbitol dehydrogenase activities were noted, but no gross or microscopic liver lestions were reported. Coumarin was found to inhibit Uvr repair of ultraviolet induced lesions in Escherichia coli. Groups of pregnant mice were fed in the diet on days 6-17 of pregnancy. No increase in malformations at any dose was noted although delayed ossification and increased still births at the high dose group was found. Groups of three male and three female Orsborne-Mendel rats were fed coumarin in the diet for four weeks. Marked growth retardation, testicular atrophy and slight to moderate liver damage was noted. Liver damage consisted of dead and dying cells, a decrease in oxyphillia and cytoplasm in the centrilobular cells and proliferation of bile ducts. One male and one female dog were given coumarin by capsures 6 days/wk for up to 16 days. The male was sacrificed in extremis after nime days and the female was found dead on day 16. The livers were yellow colored and had a nutmeg appearance. Microscopically there was marked disorganization of the lobular pattern, moderate increase in the size of liver cells, vacoulation, a large amount of diffusely distributed fat, focal necrosis, fibrosis and a very slight to moderate bile duct proliferation. The spleen was pale colored and the bone marrow was thin and fatty and the gall bladder moderately distended. Groups of 4 to 8 male baboons of several species were fed coumarin in the diet for two years. No changes in body weight were noted. Relative liver weights were increased in the high dose animals. No treatment related effects on liver histology were observed in six to ten month biopsy specimens. No biliary hyperplasia or fibrosis was seen at any dose. Marked dilation of the endoplasmic reticulum was seen upon sultrastructural examination of the liver in three high dose animals.[ |
| Source: DrugBank or Hazardous Substances Data Bank (HSDB) |
| Food Additive Safety (OFAS) |
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| COUMARIN--PROHIBITED is used for FLAVORING AGENT OR ADJUVANT. More food additive safty information please view GRAS report. |
| EFSA's chemical Hazards Database : OpenFoodTox |
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| This compound is found in OpenFoodTox with the name: Coumarin |
| Receptor | REFERENCE | EC50 [µM] | Effective Concentration [µM] |
|---|---|---|---|
| TAS2R10 | details | Activated | 300.00 |
| TAS2R14 | details | Activated | 300.00 |
| OR1C1 | details | Activated | |
| OR1G1 | details | Activated | |
| OR2B11 | details | Activated | |
| OR2J2 | details | Activated | |
| OR2J3 | details | Activated | |
| OR2W1 | details | Activated | |
| OR5P3 | details | Activated |