Petals of red chrysanthemum (Dendranthema grandiflorum) are habitually eaten in Japan. In the present study, plasma concentration profiles of two major acylated anthocyanins derived from the petals of red chrysanthemum were evaluated in rats after oral administration of an anthocyanin-rich fraction obtained from red chrysanthemum. The structures of the two major anthocyanins in the petals of red chrysanthemum were determined to be cyanidin 3-O-β-D-(3″, 6″-di-O-malonyl)-glucopyranoside and cyanidin 3-O-β-D-(6″-mono-O-malonyl)- glucopyranoside. Both malonyl anthocyanins were quickly absorbed from the gastrointestinal tract and were detected in rat blood plasma in their original acylated forms 15 min after the oral administration of the anthocyanin fraction obtained from the petals of red chrysanthemum. The absorption amounts of anthocyanins evaluated from the area under the plasma concentration curves during 8 h normalized to the orally administered dose were in the following order: cyanidin 3-O-β-D-(3″, 6″-di-O-malonyl)-glucopyranoside > cyanidin 3-O-β-D-(6″-mono-O-malonyl)-glucopyranoside > cyanidin 3-O-β-D-glucopyranoside. The present results demonstrated that the additional malonylation of the glucopyranosyl moiety of position 3″ and 6″ of cyanidin 3-O-β-D-glucopyranoside enhanced the intestinal absorption of anthocyanins.

Selenium (Se) is an essential biological element and selenite is used to supplement malnutrition of Se and may also have anticancer activity. However, Se is also known as a delicate micronutrient with a narrow window of useful dose and the mechanisms for the sudden toxic effect remain unclear. Recently, we reported elsewhere that selenite was incorporated into cells via xCT, a cystine/glutamate antiporter. xCT is regulated by a stress responsive nuclear factor erythroid 2-related factor 2 (Nrf2). Therefore, we hypothesized and preliminary substantiated that the Nrf2-xCT pathway underlies the toxicity mechanism of Se. Expression of xCT mRNA was remarkably increased in MCF-7 cells after Se treatment, which may further increase Se uptake and oxidative stress. Pretreatment with xCT or Nrf2 inhibitors prevented morphological changes by releasing cells from uncontrolled feedback on Se uptake. Paradoxically, Se-induced oxidative toxicity is promoted by a runaway of stress response in Nrf2-xCT pathway. The results imply a novel mechanism by which Se accelerates its oxidative toxicity through feedback via Nrf2-xCT. This mechanism explain the elusive toxicological properties of inorganic Se, including strong cytotoxicity, high sensitivity in cancer cells, and narrowness of pharmacological dose range.

Nanoparticles are concerned to show adverse biological effects despite their unique functions. Their physicochemical properties and status are widely diverse; this makes safety analysis of nanoparticles complicated. Some reports showed that nanoparticles could disturb acquired immunity, while it is still unclear what is the inducer of that effects. Here, we tried to explore the relationship among nanoparticles' physicochemical properties and sensitizing potential by using the human cell line activation test based in vitro method; that uses in expression of CD86 and CD54 as an index of cellular activation. As a model of nanoparticles, we examined sensitization potential of silica particles with or without a human protein corona. Of the cells treated with silica particles (diameter: 50 or 300 nm) only, none of them showed activation. On the other hand, silica particles with human protein corona showed activation. Moreover, protein corona that forms around 50 nm silica nanoparticles have a higher sensitization potential than that of protein corona that forms around 300 nm silica particles. Our findings indicated that silica particles with human protein corona showed sensitization potential, and that sensitization potential could depend on the amount or kind of proteins within the corona.