Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.
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provides coniferyl ferulate(CAS#:29706-59-0) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
Sulfotransferase 1A (SULT1A) expression is lower in the liver of humans than that of rodents. Therefore, species differences should be taken into consideration when assessing the risk of rodent hepatocarcinogens metabolically activated by SULT1A in humans. Although some renal carcinogens require SULT1A-mediated activation, it is unclear how SULT1A activity in the liver affects renal carcinogens. To explore the effects of SULT1A activity in the liver on genotoxicity induced by SULT1A-activated renal carcinogens, B6C3F1 mice or gpt delta mice of the same strain background were given lucidin-3-O-primeveroside (LuP), a hepatic and renal carcinogen of rodents, for 4 or 13 weeks, respectively, and pentachlorophenol (PCP) as a liver-specific SULT inhibitor, was given from 1 week before LuP treatment to the end of the experiment. A 4 week exposure of LuP induced lucidin-specific DNA adduct formation. The suppression of Sult1a expression was observed only in the liver but not in the kidneys of PCP-treated mice, but co-administration of PCP suppressed LuP-induced DNA adduct formation in both organs. Thirteen-week exposure of LuP increased mutation frequencies and cotreatment with PCP suppressed these increases in both organs. Given that intact levels of SULT activity in the liver were much higher than in the kidneys of rodents, SULT1A may predominantly activate LuP in the liver, consequently leading to genotoxicity not only in the liver but also in the kidney. Thus, species differences should be considered in human risk assessment of renal carcinogens activated by SULT1A as in the case of the corresponding liver carcinogens.
DNA adduct; gene mutation; lucidin-3-O-primeveroside; sulfotransferase.
Effects of inhibition of hepatic sulfotransferase activity on renal genotoxicity induced by lucidin-3-O-primeveroside
Yuji Ishii 1, Aki Kijima 1, Shinji Takasu 1, Kumiko Ogawa 1, Takashi Umemura 1 2
Lucidin-3-O- primeveroside (LuP) is one of the components of madder root (Rubia tinctorum L.; MR) which is reported to be carcinogenic in the kidney and liver of rats. Since metabolism of LuP generates genotoxic compounds such as lucidin (Luc) and rubiadin (Rub), it is likely that LuP plays a key role in MR carcinogenesis. In the present study, the chemical structures of Luc-specific 2′-deoxyguanosine (dG) and 2′-deoxyadenosine (dA) adducts following the reactions of dG and dA with a Luc carbocation or quinone methide intermediate derived from Acetoxy-Luc were determined by liquid chromatography with photodiode array and electron spray ionizaion-mass spectrometry (LC-PDA-ESI/MS). The identification of the two measurable adducts as Luc-N(2)-dG and Luc-N(6)-dA was confirmed by NMR analysis. Subsequently, using a newly developed quantitative analytical method using LC-ESI/MS, the formation of Luc-N(2)-dG and Luc-N(6)-dA from the reaction of calf thymus DNA with Luc in the presence of S9 mixture was observed. The fact that this reaction with Rub also gave rise to the same dG and dA adducts strongly suggests that Rub genotoxicity involves a metabolic conversion to Luc. The precise determination of the modified DNA bases generated by LuP and the method for their analysis may contribute to further comprehension of the mode of action underlying carcinogenesis by MR and related anthraquinones.
Chemical structure determination of DNA bases modified by active metabolites of lucidin-3-O-primeveroside
Yuji Ishii 1, Toshiya Okamura, Tomoki Inoue, Kiyoshi Fukuhara, Takashi Umemura, Akiyoshi Nishikawa
Rubia tinctorum L., a medicinal plant used for the treatment of kidney and bladder stones, contains a characteristic spectrum of 9,10-anthraquinone derivatives, which are substituted in only one of the aromatic benzo rings. The majority of the anthraquinones present in the plant itself or in plant extracts are glycosides. We investigated the metabolism of two such glycosides, alizarinprimeveroside (AlP) and lucidinprimeveroside (LuP). AlP given orally to rats was metabolized to alizarin (Al) and 1-hydroxyanthraquinone (1-HA). The reductive cleavage of AlP was also observed after treatment of this compound with rat liver enzymes (S9) and NADPH. 1-HA has been reported to induce unscheduled DNA synthesis (UDS) in primary rat hepatocytes (PRH) and intestinal and liver tumors in rats after chronic treatment. The in vitro genotoxicity of 1-HA was confirmed by our present investigations. We also observed that the glycoside AlP was active at inducing UDS in PRH, but the compound was inactive in the Salmonella/microsome assay. Oral administration of LuP to rats resulted in the excretion of lucidin and rubiadin. When LuP was treated with rat liver extract and NADPH, the compound was reduced to rubiadinprimeveroside (RuP), which was hydrolyzed to rubiadin. We have recently shown that lucidin is highly genotoxic in a battery of short-term tests. We now report that rubiadin is also highly genotoxic in Salmonella typhimurium. However, in contrast to lucidin, it requires metabolic activation. In the UDS assay in PRH, rubiadin was even more potent than lucidin and equal to the positive control DMBA. In addition, the glycoside LuP is active in the Salmonella/microsome assay as well as in the UDS assay. The present work demonstrates that the uptake of the anthraquinone glycosides AlP and LuP leads to the rodent carcinogen 1-HA, and to the highly genotoxic compounds lucidin and rubiadin. This extends our previous studies and supports our suggestion that the therapeutic use of Rubia tinctorum may involve a carcinogenic risk.
Formation of genotoxic metabolites from anthraquinone glycosides, present in Rubia tinctorum L
B Blomeke 1, B Poginsky, C Schmutte, H Marquardt, J Westendorf