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With the aim of contributing to the knowledge about their potential therapeutic activity, we determined the biological activities of cyanidin and its selected O-glycosides in relation to erythrocytes (RBCs) and human dermal vascular endothelial cells (HMEC-1). Furthermore, on the basis of changes in the physical/functional properties of the cells, the structure–activity relationships of the compounds were determined. Concerning erythrocytes, we analyzed the antioxidant activity of the compounds and their impact on the RBCs’ shape and transmembrane potential. The compounds’ cytotoxic activity, ability to modulate apoptosis, cell cycle, and intracellular ROS generation, as well as inhibitory activity against AAPH-inducted oxidative stress, were determined in relation to HMEC-1 cells. We demonstrated that biological activity of cyanidin and its O-glycosides strongly depends on the number and type of sugar substituents, and varies depending on the extracellular environment and type of cells. The compounds are practically non-cytotoxic, and do not induce apoptosis or disturb the progression of the cell cycle. Additionally, the compounds alter the shape of RBCs, but they do not affect their transmembrane potential. They effectively protect erythrocytes against free radicals and affect intracellular reactive oxygen spices (ROS) generation under physiological and AAPH-induced oxidative stress conditions. Our results suggest a potential beneficial effect of cyanidin on the cardiovascular system.

In recent years, the development of nanotechnology opens up new prospects for biomedical applications of unmodified and chemically modified diamond nanoparticles (DNPs). The problem of biocompatibility of DNPs is thus of primary importance. The first step in the modification of DNPs is usually the introduction of -OH groups, which can bind other functional groups. One of the basic methods to introduce -OH groups onto DNPs is the Fenton reaction. The aim of this study was to compare the effect of unmodified DNPs and nanoparticles modified by the Fenton reaction on human endothelial cells. Ultradisperse diamond (UDD) was modified by the Fenton reaction introducing surface -OH groups. Immortalized human umbilical cord endothelial cells (HUVEC-ST) were incubated with 2-100 µg/mL nanopowders in the opti-MEM medium. For comparison, graphite powder (GRAF and GRAF+OH) was also employed. UDD and GRAF augmented generation of reactive oxygen species in the cells after 24 H incubation, estimated by oxidation of 2',7'-dichlorofluorescin diacetate (H2DCF-DA). Cellular production of nitric oxide, estimated with DAF-FM-DA (3-amino-4-aminomethyl 2',7'-dichlorofluorescein diacetate), was also affected by UDD and GRAF after 24 H. Fenton-modified OH, in contrast to unmodified diamond, decreased NO production. Detonation nanoparticles also affected the cellular content of glutathione and activities of main antioxidant enzymes (superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, and glutathione S-transferase). This article was published online on 5 February 2013. Errors in the byline and affiliation line were subsequently identified. This notice is included in the online and print versions to indicate that both have been corrected 18 April 2013.

Diamond nanoparticles find numerous applications in pharmacy, medicine, cosmetics, and biotechnology. However, possible adverse cellular effects of diamond nanoparticle cells have been reported, which may limit their use. The aim of this study was to compare the effect of nonmodified diamond nanoparticles (D) and diamond nanoparticles modified by the Fenton reaction (D+OH) on human umbilical cord endothelial cells (HUVEC-ST). We found that both D and D+OH show time- and concentration-dependent cytotoxicity, inducing apoptosis and necrosis of HUVEC-ST. Interaction with D and D+OH also induced changes in the production of reactive oxygen and nitrogen species and changes in the level of glutathione and activities of antioxidant enzymes in the cells. These data demonstrate that diamond nanoparticles may induce oxidative stress in human endothelial cells, which contributes to their cytotoxic effects seen at higher concentrations of D and D+OH.