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Restrict the search for
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Status:
Other
Class (Stereo):
CHEMICAL (ABSOLUTE)
Aloesin is a chromone derivative isolated from aloe vera. It has many biological effects, such as wound and burn healing properties, and antioxidant, free radical scavenging, anti-inflammatory, and immunomodulatory effects. Aloesin has been shown to be a potent and selective inhibitor of tyrosinase. It exhibited direct inhibitory effects on melanogenesis. Aloesin treatment showed pigmentation suppression in a dose-dependent manner. Thus, aloesin may be used as an agent that inhibits melanin formation induced by UV radiation. Aloesin is thought to be one of the active ingredients in regards to the anti-diabetic activity of Aloe. Aloesin exerts its anticancer effect through the MAPK signaling pathway. It is a novel therapeutic drug for ovarian cancer treatment.
Status:
Other
Class (Stereo):
CHEMICAL (ABSOLUTE)
Gingerol (6-Gingerol) is bioactive compound found in ginger (Zingiber officinale) with antioxidant activity, which functions as an anti-inflammatory and antitumor agent. 6-Gingerol has been found to possess anticancer activities via its effect on a variety of biological pathways involved in apoptosis, cell cycle regulation, cytotoxic activity, and inhibition of angiogenesis. Gingerol has been investigated for its effect on cancerous tumors in the bowel, breast tissue, ovaries, the pancreas, among other tissues, with positive results. In phase II clinical trials Gingerol was successfully studied for preventing chemotherapy- induced nausea and vomiting in patients receiving highly emetogenic chemotherapy.
Ponceau xylidine is a component of the Masson's trichrome stain as a red counterstain.
BENZYL VIOLET had long been used as a food color in some countries including Japan. It had been classified as "possibly carcinogenic to humans" compounds by the International Agency for Research on Cancer (IARC) and by the Japan Society for Occupational Health. It was deleted from the food additives list in Japan in December 1972.
Status:
Other
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Ellipticine (5,11-dimethyl-6H-pyrido[4,3-b]carbazole), an alkaloid isolated from Apocyanaceae plants (i.e. Ochrosia borbonica, Excavatia coccinea), and several its derivatives exhibit significant antitumor and anti-HIV activities. This compound is one of the simplest naturally occurring alkaloids, having a planar structure. It was first isolated in 1959 from the leaves of the evergreen tree Ochrosia elliptica, which grows wild in Oceania. Ellipticine and its more soluble derivatives (9-hydroxyellipticine, 9-hydroxy-N2-methylellipticinium, 9-chloro-N2 -methylellipticinium and 9-methoxy-N2 -methylellipticinium) exhibit promising results for the treatment of osteolytic breast cancer metastases, kidney cancer, brain tumors and acute myeloblastic leukemia. The main reason for the interest in ellipticine and its derivatives for clinical purposes is their high efficiencies against several types of cancer, their rather limited toxic side effects and their complete lack of hematological toxicity. Nevertheless, the mutagenicity of ellipticines should be evaluated as a potential risk factor for these anticancer agents. Most ellipticines are mutagenic to Salmonella typhimurium Ames tester strains, bacteriophage T4, Neurospora crassa, and mammalian cells and induce prophage lambda in Escherichia coli. The anti-tumor therapeutic ellipticine and its derivatives act as potent anticancer agents via a combined mechanism involving cell cycle arrest and induction of apoptosis. Cell death induced by ellipticine has been shown to engage a p53-dependent pathway, cell cycle arrest, interaction with several kinases and induction of the mitochondrial pathway of apoptotic cell death. Cell cycle arrest was shown to result from DNA damage caused by a variety of tumor chemotherapeutic agents; this is also the case for ellipticines. The prevalent DNA-mediated mechanisms of anti-tumor, mutagenic and cytotoxic activities of ellipticine are (i) intercalation into DNA, (ii) inhibition of DNA topoisomerase II activity, and (iii) covalent binding to DNA in vitro and in vivo after enzymatic activation by cytochrome P450 and/or peroxidase enzymes The mechanism leading to apoptosis by ellipticine is thought to also be associated with DNA damage, by inhibition of topoisomerase II and the covalent modification of DNA. In addition, the formation of ellipticine-DNA adducts ultimately can mutate cancer cells or initiate cell death.
Status:
Other
Class (Stereo):
CHEMICAL (RACEMIC)
Targets:
Conditions:
Selenomethionine, DL- is the racemic mixture of the D and L enantiomers of Selenomethionine, that used us animal’s dietary supplement. Selenomethionine, DL- was tolerated by chickens for fattening at up to 1.5 mg selenium supplemented/kg feed; Selenomethionine, DL- is therefore safe for chickens for fattening provided total dietary selenium does not exceed 0.5 mg/kg complete feed; this conclusion is extended to all animal species. Based on available toxicity studies and previous assessments of closely related compounds, it is concluded that selenium from Selenomethionine, DL- does not elicit any adverse effects not expected in a selenium compound. The use of Selenomethionine, DL- in animal nutrition is expected to result in a similar increase in selenium deposition in animal tissues/products as that resulting from other sources of Selenomethionine, DL- . To ensure consumer safety from consumption of food originating from animals fed Selenomethionine, DL-, dietary selenium supplementation from the additive should not exceed a maximum of 0.2 mg Se/kg complete feed. Although a Selenomethionine, DL- containing additive did not release any measurable dust, the additive is considered as a hazard by inhalation, which requires protection measures for users since the additive is not the subject of authorisation, and selenium is highly toxic. The additive is not an irritant to skin and eyes and is not a dermal sensitiser. The use of Selenomethionine, DL- in feed does not pose an additional risk to the environment, compared with other sources of selenium for which it will substitute, as long as the maximum authorised content in complete feed is not exceeded.
