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Items 1 to 11 of about 11
2. National Toxicology Program: NTP technical report on the toxicology and carcinogenesis studies of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) (CAS No. 1746-01-6) in female Harlan Sprague-Dawley rats (Gavage Studies). Natl Toxicol Program Tech Rep Ser; 2006 Apr;(521):4-232
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Structurally related compounds that bind to the AhR and exhibit biological actions similar to TCDD are commonly referred to as "dioxin-like compounds" (DLCs).
  • The main sources of TCDD releases into the environment are from combustion and incineration; metal smelting, refining, and processing; chemical manufacturing and processing; biological and photochemical processes; and existing reservoir sources that reflect past releases.
  • HEPATIC CELL PROLIFERATION DATA: To evaluate hepatocyte replication, analysis of labeling of replicating hepatocytes with 5-bromo-2'-deoxyuridine was conducted at the 14-, 31-, and 53-week interim evaluations.
  • DETERMINATIONS OF TCDD CONCENTRATIONS IN TISSUES: The tissue disposition of TCDD was analyzed in the liver, lung, fat, and blood of all animals in each group at the 14-, 31-, and 53-week interim evaluations and in 10 animals per group at the end of the 2-year study (105 weeks).
  • Exposure led to a treatment-related increase in hepatic toxicity with a broad spectrum of lesions.
  • At 2 years, there was a significant increase in toxic hepatopathy characterized by increased incidences of numerous nonneoplastic liver lesions including hepatocyte hypertrophy, multinucleated hepatocytes, altered hepatocellular foci, inflammation, pigmentation, diffuse fatty change, necrosis, portal fibrosis, oval cell hyperplasia, bile duct hyperplasia, bile duct cysts, cholangiofibrosis, and nodular hyperplasia At 2 years, the incidence of hepatocellular adenoma was significantly increased in the 100 ng/kg core study group.
  • The highest incidence of cholangiocarcinoma was seen in the 100 ng/kg core study group and included a significant number of animals with multiple cholangiocarcinomas.
  • The incidence of gingival squamous cell carcinoma of the oral mucosa was significantly increased in the 100 ng/kg core study group at 2 years and was accompanied by an increased incidence of gingival squamous hyperplasia.
  • At 2 years, the incidence of squamous cell carcinoma of the uterus in the 46 ng/kg group was significantly increased, and there were two squamous cell carcinomas in the 100 ng/kg stop-exposure group.
  • At 2 years, one acinar adenoma and two acinar cell carcinomas of the pancreas were seen in the 100 ng/kg core study group; one acinar carcinoma was seen in the 100 ng/kg stop-exposure group.
  • The incidences of acinar cell adenoma or carcinoma (combined) exceeded the historical vehicle control range.
  • Nonneoplastic effects in the lung included acinar cytoplasmic vacuolization, chronic active inflammation, acinar atrophy, and arterial chronic active inflammation. (ABSTRACT TRUNCATED)
  • [MeSH-minor] Animals. Body Weight / drug effects. Carcinogenicity Tests. Female. Mice. Neoplasms, Experimental / chemically induced. Organ Size / drug effects. Rats. Rats, Sprague-Dawley

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  • (PMID = 16835633.001).
  • [ISSN] 0888-8051
  • [Journal-full-title] National Toxicology Program technical report series
  • [ISO-abbreviation] Natl Toxicol Program Tech Rep Ser
  • [Language] eng
  • [Publication-type] Journal Article; Technical Report
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinogens; DO80M48B6O / Tetrachlorodibenzodioxin
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3. Fourni JW, Hawkins WE: Exocrine pancreatic carcinogenesis in the guppy Poecilia reticulata. Dis Aquat Organ; 2002 Dec 10;52(3):191-8
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  • Pancreatic acinar cell adenomas and carcinomas occurred in 42 of 243 (17%) of the specimens exposed to MAM-Ac.
  • Acinar cell adenomas accounted for 27 of the 42 neoplasms.
  • Adenomas exhibited a high degree of acinar cell differentiation and some contained foci of atypical acinar cells that were less differentiated and more basophilic than were surrounding adenoma cells.
  • [MeSH-major] Adenoma / veterinary. Carcinoma, Acinar Cell / veterinary. Fish Diseases / chemically induced. Methylazoxymethanol Acetate / toxicity. Pancreatic Neoplasms / veterinary. Poecilia. Water Pollutants, Chemical / toxicity
  • [MeSH-minor] Animals. Dose-Response Relationship, Drug. Pancreas / pathology. Time Factors

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  • (PMID = 12553447.001).
  • [ISSN] 0177-5103
  • [Journal-full-title] Diseases of aquatic organisms
  • [ISO-abbreviation] Dis. Aquat. Org.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Water Pollutants, Chemical; 592-62-1 / Methylazoxymethanol Acetate
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4. Sahin F, Kannangai R, Adegbola O, Wang J, Su G, Torbenson M: mTOR and P70 S6 kinase expression in primary liver neoplasms. Clin Cancer Res; 2004 Dec 15;10(24):8421-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • This study was undertaken to determine the prevalence and clinicopathological correlates of mTOR pathway activation in hepatocellular carcinoma and to determine whether rapamycin inhibits the pathway in cell culture.
  • Results were correlated with tumor growth pattern as defined by the WHO (trabecular, pseudoglandular/acinar, compact, and scirrhous), tumor size, Ki-67 proliferation index, and the modified Edmondson nuclear grade, which has a scale of 1 to 4.
  • HepG2 and Hep3B cell lines were treated with rapamycin to see the effect on proliferation and S6K phosphorylation.
  • Rapamycin treatment of HepG2 and Hep3B cell lines markedly inhibited cell proliferation and reduced S6K phosphorylation in both cell lines.
  • Rapamycin can inhibit proliferation of neoplastic hepatocytes in cell culture.
  • [MeSH-minor] Adenoma / metabolism. Adenoma / pathology. Antibiotics, Antineoplastic / pharmacology. Carcinoma, Hepatocellular / metabolism. Carcinoma, Hepatocellular / pathology. Cell Proliferation / drug effects. Female. Genetic Heterogeneity. Hepatitis / metabolism. Hepatitis / pathology. Humans. Immunoenzyme Techniques. Ki-67 Antigen / metabolism. Male. Middle Aged. Phosphorylation / drug effects. Sirolimus / pharmacology. TOR Serine-Threonine Kinases. Tumor Cells, Cultured / drug effects

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  • (PMID = 15623621.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Ki-67 Antigen; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.11.1 / Ribosomal Protein S6 Kinases, 70-kDa; W36ZG6FT64 / Sirolimus
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5. National Toxicology Program: Toxicology and carcinogenesis studies of 2,3',4,4',5-pentachlorobiphenyl (PCB 118) (CAS No. 31508-00-6) in female harlan Sprague-Dawley rats (gavage studies). Natl Toxicol Program Tech Rep Ser; 2010 Nov;(559):1-174

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Structurally related compounds that bind to the AhR and exhibit biological actions similar to TCDD are commonly referred to as "dioxin-like compounds"(DLCs).
  • Manufacture and use of these chemicals were stopped because of increased PCB residues in the environment, but they continue to be released into the environment through the use and disposal of products containing PCBs, as by-products during the manufacture of certain organic chemicals, during combustion of some waste materials, and during atmospheric recycling.
  • In general, exposure to PCB 118 lead to dose-dependent decreases in the concentrations of serum total thyroxine (T4) and free T4 in all dosed groups.
  • There were increases in hepatic cell proliferation in the 4,600 g/kg group at 14, 31, and 53 weeks.
  • Administration of PCB 118 led to dose-dependent increases in CYP1A1-associated 7-ethoxyresorufin-O-deethylase, CYP1A2-associated acetanilide4-hydroxylase, and CYP2B-associated pentoxyresorufin-O-deethylase activities at the 14-, 31-, and 53-week interim evaluations.
  • Analysis of PCB 118 concentrations in dosed groups showed dose- and duration of dosing-dependent increases in fat, liver, lung, and blood.
  • At the 53-week interim evaluation, three 4,600 g/kg rats had liver cholangiocarcinoma and one had hepatocellular adenoma.
  • At 2 years, there were significant treatment-related increases in the incidences of cholangiocarcinoma and hepatocellular adenoma.
  • At 2 years, a significant dose-related increase in hepatic toxicity was observed and was characterized by increased incidences of numerous lesions including hepatocyte hypertrophy, inflammation, oval cell hyperplasia, pigmentation, multinucleated hepatocyte, eosinophilic and mixed cell foci, diffuse fatty change, toxic hepatopathy, nodular hyperplasia, necrosis, bile duct hyperplasia and cyst, and cholangiofibrosis.
  • A marginal increase in squamous cell carcinoma occurred in the 220 g/kg group.
  • At 2 years, there were marginally increased incidences of exocrine pancreatic adenoma or carcinoma in the 460, 1,000, and 4,600 g/kg core study groups.
  • Numerous nonneoplastic effects were seen in other organs including: adrenal cortical atrophy and cytoplasmic vacuolization, pancreatic acinar cell cytoplasmic vacuolization and arterial chronic active inflammation, follicular cell hypertrophy of the thyroid gland, inflammation and respiratory epithelial hyperplasia of the nose, and kidney pigmentation.
  • CONCLUSIONS: Under the conditions of this 2-year gavage study, there was clear evidence of carcinogenic activity of PCB 118 in female Harlan Sprague-Dawley rats based on increased incidences of neoplasms of the liver (cholangiocarcinoma, hepatocholangioma, and hepatocellular adenoma) and cystic keratinizing epithelioma of the lung.
  • Occurrences of squamous cell carcinoma of the uterus and acinar neoplasms of the pancreas may have been related to administration of PCB 118.
  • [MeSH-minor] Animals. Carcinogenicity Tests. Dose-Response Relationship, Drug. Female. Humans. Male. Rats. Rats, Sprague-Dawley. Tetrachlorodibenzodioxin / toxicity

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  • (PMID = 21383778.001).
  • [ISSN] 0888-8051
  • [Journal-full-title] National Toxicology Program technical report series
  • [ISO-abbreviation] Natl Toxicol Program Tech Rep Ser
  • [Language] eng
  • [Publication-type] Journal Article; Technical Report
  • [Publication-country] United States
  • [Chemical-registry-number] 31508-00-6 / 2,3',4,4',5-pentachlorobiphenyl; DFC2HB4I0K / Polychlorinated Biphenyls; DO80M48B6O / Tetrachlorodibenzodioxin
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7. Cheuk DK, Shek TW, Chan GC, Lau YL, Ha SY, Chiang AK: Parotid acinar cell carcinoma in a long-term survivor of childhood acute lymphoblastic leukemia. Pediatr Blood Cancer; 2008 Mar;50(3):636-9
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  • [Title] Parotid acinar cell carcinoma in a long-term survivor of childhood acute lymphoblastic leukemia.
  • We report the clinical and pathological features of a rarer histological type, acinic cell carcinoma (ACC), in a childhood acute lymphoblastic leukemia (ALL) survivor.
  • Careful monitoring for recurrence or a third malignancy is needed.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Carcinoma, Acinar Cell / etiology. Neoplasms, Radiation-Induced / etiology. Neoplasms, Second Primary / etiology. Parotid Neoplasms / etiology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Whole-Body Irradiation / adverse effects
  • [MeSH-minor] 6-Mercaptopurine / administration & dosage. 6-Mercaptopurine / adverse effects. Adenoma, Sweat Gland / etiology. Adenoma, Sweat Gland / surgery. Asparaginase / administration & dosage. Asparaginase / adverse effects. Child, Preschool. Combined Modality Therapy / adverse effects. Cyclophosphamide / administration & dosage. Cyclophosphamide / adverse effects. Cytarabine / administration & dosage. Cytarabine / adverse effects. Daunorubicin / administration & dosage. Daunorubicin / adverse effects. Epirubicin / administration & dosage. Epirubicin / adverse effects. Etoposide / administration & dosage. Etoposide / adverse effects. Follow-Up Studies. Humans. Male. Methotrexate / administration & dosage. Methotrexate / adverse effects. Prednisolone / administration & dosage. Prednisolone / adverse effects. Recurrence. Remission Induction. Survivors. Sweat Gland Neoplasms / etiology. Sweat Gland Neoplasms / surgery. Vincristine / administration & dosage. Vincristine / adverse effects

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 16865683.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 3Z8479ZZ5X / Epirubicin; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 8N3DW7272P / Cyclophosphamide; 9PHQ9Y1OLM / Prednisolone; E7WED276I5 / 6-Mercaptopurine; EC 3.5.1.1 / Asparaginase; YL5FZ2Y5U1 / Methotrexate; ZS7284E0ZP / Daunorubicin; UKALL X protocol
  • [Number-of-references] 17
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8. David RM, Moore MR, Finney DC, Guest D: Chronic toxicity of di(2-ethylhexyl)phthalate in rats. Toxicol Sci; 2000 Jun;55(2):433-43
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Blood and urine were analyzed at weeks 26, 52, 78, and 104 from 10 animals per sex per group.
  • Bilateral aspermatogenesis in the testes, castration cells in the pituitary gland, spongiosis hepatis, and pancreatic acinar cell adenoma were observed for 12,500-ppm male rats.
  • Kupffer cell pigmentation and renal tubule pigmentation were seen in male and female 12,500-ppm rats.
  • The increased incidence of spongiosis hepatis correlated with increased palmitoyl CoA oxidase activity, but the incidence of pancreatic acinar cell adenoma was increased only at the highest dose level of 12,500 ppm.
  • [MeSH-minor] Adenoma / chemically induced. Adenoma / pathology. Animals. Blood Urea Nitrogen. Body Weight / drug effects. Eating / drug effects. Erythrocyte Count / drug effects. Female. Hematocrit. Hemoglobins / drug effects. Kidney / drug effects. Kidney / pathology. Liver / drug effects. Liver / pathology. Male. Organ Size / drug effects. Pancreatic Neoplasms / chemically induced. Pancreatic Neoplasms / pathology. Peroxisome Proliferators / toxicity. Rats. Rats, Inbred F344. Serum Albumin / drug effects. Serum Globulins / drug effects. Toxicity Tests

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  • (PMID = 10828276.001).
  • [ISSN] 1096-6080
  • [Journal-full-title] Toxicological sciences : an official journal of the Society of Toxicology
  • [ISO-abbreviation] Toxicol. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Hemoglobins; 0 / Peroxisome Proliferators; 0 / Serum Albumin; 0 / Serum Globulins; C42K0PH13C / Diethylhexyl Phthalate
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9. Richart J, Brunt EM, Di Bisceglie AM: Expression of P-glycoprotein and C-MOAT in human hepatocellular carcinoma: detection by immunostaining. Dig Dis Sci; 2002 Nov;47(11):2454-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • P-Glycoprotein and C-MOAT are important hepatic transport proteins which play a role in handling anticancer drugs.
  • Hepatocellular carcinoma is a common hepatic malignancy that is relatively resistant to chemotherapeutic drugs.
  • We therefore studied the expression of these two transport proteins in liver sections from hepatocellular carcinoma by immunohistochemistry and compared the reactivity to that in other liver conditions, including cirrhosis and dysplasia.
  • We studied 53 sections from 17 liver specimens and found that the majority of samples stained positively for both P-glycoprotein and C-MOAT; however, the degree of staining was less in HCC and hepatic adenoma than in liver adjacent to HCC or in cirrhosis or dysplastic nodules.
  • HCC with a compact pattern had less staining than those with acinar, scirrhous, or trabecular patterns.
  • [MeSH-major] Carcinoma, Hepatocellular / metabolism. Liver / metabolism. Liver Neoplasms / metabolism. Multidrug Resistance-Associated Proteins / metabolism. P-Glycoprotein / metabolism
  • [MeSH-minor] Adenoma / metabolism. Humans. Immunohistochemistry. Liver Cirrhosis / metabolism

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  • [Cites] J Cell Sci. 1991 Mar;98 ( Pt 3):317-22 [1676033.001]
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  • (PMID = 12452378.001).
  • [ISSN] 0163-2116
  • [Journal-full-title] Digestive diseases and sciences
  • [ISO-abbreviation] Dig. Dis. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ABCC5 protein, human; 0 / Multidrug Resistance-Associated Proteins; 0 / P-Glycoprotein
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10. Biegel LB, Hurtt ME, Frame SR, O'Connor JC, Cook JC: Mechanisms of extrahepatic tumor induction by peroxisome proliferators in male CD rats. Toxicol Sci; 2001 Mar;60(1):44-55
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  • Wyeth-14,643 (WY) and ammonium perfluorooctanoate (C8) belong to a diverse class of compounds which have been shown to produce hepatic peroxisome proliferation in rodents.
  • From previous work, WY, but not C8, has been shown to produce hepatocellular carcinoma in rats, while C8 has been shown to produce Leydig cell adenomas.
  • In addition, based on a review of bioassay data a relationship appears to exist between peroxisome-proliferating compounds and Leydig cell adenoma and pancreatic acinar cell hyperplasia/adenocarcinoma formation.
  • To further investigate the relationship between peroxisome-proliferating compounds and hepatic, Leydig cell, and pancreatic acinar cell tumorigenesis, a 2-year feeding study in male CD rats was initiated to test the hypothesis that peroxisome proliferating compounds induce a tumor triad (liver, Leydig cell, pancreatic acinar cell), and to examine the potential mechanism for the Leydig cell tumors.
  • Peroxisome proliferation measured by beta-oxidation activity and cell proliferation were measured in the liver and testis at all time points and in the pancreas beginning at the 9-month time point (cell proliferation only).
  • In contrast, hepatic cell proliferation was significantly increased only in the WY-treated group.
  • Neither WY nor C8 significantly altered the rate of Leydig cell beta-oxidation or Leydig cell proliferation when compared to the control groups.
  • Histopathological evaluation revealed compound-related increases in liver, Leydig cell, and pancreatic acinar cell tumors in both WY- and C8-treated rats.
  • In addition, both C8 and WY produced a sustained increase in serum estradiol concentrations that correlated with the potency of the 2 compounds to induce Leydig cell tumors (i.e., WY caused a more consistent sustained increase in serum estradiol throughout the entire study, and more specifically at the end of the study, than did C8).
  • This study suggests that estradiol may play a role in enhancement of Leydig cell tumors in the rat, and that peroxisome proliferators may induce tumors via a non-LH type mechanism.
  • [MeSH-minor] Adenocarcinoma / chemically induced. Adenocarcinoma / pathology. Animals. Carcinogenicity Tests. Cell Division / drug effects. Diet. Estradiol / blood. Follicle Stimulating Hormone / blood. Leydig Cell Tumor / chemically induced. Leydig Cell Tumor / pathology. Liver / drug effects. Liver / pathology. Liver Neoplasms / chemically induced. Liver Neoplasms / pathology. Longevity / drug effects. Luteinizing Hormone / blood. Organ Size / drug effects. Pancreatic Neoplasms / chemically induced. Pancreatic Neoplasms / pathology. Prolactin / blood. Rats. Rats, Inbred Strains. Testosterone / blood

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  • (PMID = 11222872.001).
  • [ISSN] 1096-6080
  • [Journal-full-title] Toxicological sciences : an official journal of the Society of Toxicology
  • [ISO-abbreviation] Toxicol. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Caprylates; 0 / Carcinogens; 0 / Fluorocarbons; 0 / Peroxisome Proliferators; 0 / Pyrimidines; 3XMK78S47O / Testosterone; 4TI98Z838E / Estradiol; 86C4MRT55A / pirinixic acid; 9002-62-4 / Prolactin; 9002-67-9 / Luteinizing Hormone; 9002-68-0 / Follicle Stimulating Hormone; 947VD76D3L / perfluorooctanoic acid
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11. Johnson W Jr, Cosmetic Ingredient Review Expert Panel: Final report on the safety assessment of trilaurin, triarachidin, tribehenin, tricaprin, tricaprylin, trierucin, triheptanoin, triheptylundecanoin, triisononanoin, triisopalmitin, triisostearin, trilinolein, trimyristin, trioctanoin, triolein, tripalmitin, tripalmitolein, triricinolein, tristearin, triundecanoin, glyceryl triacetyl hydroxystearate, glyceryl triacetyl ricinoleate, and glyceryl stearate diacetate. Int J Toxicol; 2001;20 Suppl 4:61-94
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Triesters of glycerin and aliphatic acids, known generically as glyceryl triesters and specifically as Trilaurin, etc., are used in cosmetic products as occlusive skin-conditioning agents and/or nonaqueous viscosity-increasing agents.
  • Hundreds of glyceryl triesters are used in a wide variety of cosmetic products at concentrations ranging from a few tenths of a percent to 46%.
  • Glyceryl triesters are also known as triglycerides; ingested triglycerides are metabolized to monoglycerides, free fatty acids, and glycerol, all of which are absorbed in the intestinal mucosa and undergo further metabolism.
  • Tricaprylin and other glyceryl triesters have been shown to increase the skin penetration of drugs.
  • In one study, subcutaneous injection of Tricaprylin in newborn mice produced more tumors in lymphoid tissue than were seen in untreated animals, whereas neither subcutaneous or intraperitoneal injection in 4- to 6-week-old female mice produced any tumors in another study.
  • Trioctanoin injected intraperitoneally in pregnant rats was associated with an increase in mammary tumors in the offspring compared to that seen in offspring of untreated animals, but similar studies in pregnant hamsters and rabbits showed no tumors in the offspring.
  • This treatment was associated with a statistically significant dose-related increase in pancreatic acinar cell hyperplasia and adenoma, but there were no acinar carcinomas, the incidence of mononuclear leukemia was less, and nephropathy findings were reduced, all compared to corn oil controls.
  • Clinical tests of Trilaurin at 36.3% in a commercial product applied to the skin produced no irritation reactions.
  • Trilaurin, Tristearin, and Tribehenin at 40%, 1.68%, and 0.38%, respectively, in commercial products were also negative in repeated-insult patch tests.
  • Tristearin at 0.32% in a commercial product induced transient, mild to moderate, ocular irritation after instillation into the eyes of human subjects.
  • Based on the enhancement of penetration of other chemicals by skin treatment with glyceryl triesters, it is recommended that care be exercised in using them in cosmetic products.
  • [MeSH-major] Consumer Product Safety. Cosmetics / toxicity. Fatty Acids / toxicity. Toxicity Tests. Triglycerides / toxicity
  • [MeSH-minor] Animals. Drug Administration Routes. Humans

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  • (PMID = 11800053.001).
  • [ISSN] 1091-5818
  • [Journal-full-title] International journal of toxicology
  • [ISO-abbreviation] Int. J. Toxicol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cosmetics; 0 / Fatty Acids; 0 / Triglycerides
  • [Number-of-references] 135
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