lucidin/carcinogenesis

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Characterization of lucidin formation in Rubia tinctorum L.

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In order to approach lucidin formation (a strong mutagen or a carcinogen) from a physiological standpoint, hairy roots of Rubia tinctorum L. were established by a transformation of Agrobacterium rhizogenes strain 15834 and cultured in a liquid woody plant medium without plant hormones. The

Synthesis and polymerase-mediated bypass studies of the N2-deoxyguanosine DNA damage caused by a lucidin analogue.

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Lucidin is a genotoxic and mutagenic hydroxyanthraquinone metabolite, which originates from the roots of Rubia tinctorum L. (madder root). It reacts with exocyclic amino groups of DNA nucleobases and forms adducts/lesions leading to carcinogenesis. To study the effect of lucidin-induced DNA damage,

Chemical structure determination of DNA bases modified by active metabolites of lucidin-3-O-primeveroside.

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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

Determination of lucidin-specific DNA adducts by liquid chromatography with tandem mass spectrometry in the livers and kidneys of rats given lucidin-3-O-primeveroside.

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Lucidin-3-O-primeveroside (LuP) is a component of madder color (MC), a compound which is carcinogenic in the kidney and liver of rats. Since LuP is metabolized to generate genotoxic compounds such as lucidin (Luc) and rubiadin, it is likely that these play key roles in MC carcinogenesis. In fact,

Effects of inhibition of hepatic sulfotransferase activity on renal genotoxicity induced by lucidin-3-O-primeveroside.

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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

Possible contribution of rubiadin, a metabolite of madder color, to renal carcinogenesis in rats.

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Madder color (MC) has been shown to exert carcinogenic potential in the rat kidney in association with degeneration, karyomegaly, increased cell proliferation of renal tubule cells and increased renal 8-OHdG levels. To clarify the causal relationship of components and metabolites of MC to renal

Combined application of comprehensive analysis for DNA modification and reporter gene mutation assay to evaluate kidneys of gpt delta rats given madder color or its constituents.

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DNA adductome analysis using liquid chromatography-tandem mass spectrometry is a promising tool to exhaustively search DNA modifications. Given that the molecular weight of chemical-specific adducts is determined by the total molecular weights of the active form and nucleotide bases, we developed a

Formation of genotoxic metabolites from anthraquinone glycosides, present in Rubia tinctorum L.

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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

Carcinogenic potential of alizarin and rubiadin, components of madder color, in a rat medium-term multi-organ bioassay.

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Madder color (MC), a food coloring extracted from roots of Rubia tinctorum L., has been proven to exert carcinogenicity in the rat kidney and liver. Furthermore, it induces DNA adducts in the kidney, liver, and colon. MC is in fact composed of anthraquinones such as lucidin-3-O-primeveroside and

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