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Cytotoxicity of flavonoids toward cultured normal human cells.
- M. Matsuo, N. Sasaki, K. Saga, T. Kaneko
- Biology, ChemistryBiological & pharmaceutical bulletin
- 1 February 2005
Some flavonoids are cytotoxic at higher concentrations toward human normal cells and it is suggested that they are incorporated into cells, increase intracellular ROS levels, and then exert cytotoxicity.
Retarding effect of dietary restriction on the accumulation of 8-hydroxy-2'-deoxyguanosine in organs of Fischer 344 rats during aging.
Ploidy of human embryonic fibroblasts during in vitro aging.
The saturation density of TIG-3 cells increased at the beginning of their lifespan and thereafter decreased, and the rise in their saturation density seems to reflect cell selection advantageous for young diploid cells.
Non-linear accumulation of 8-hydroxy-2'-deoxyguanosine, a marker of oxidized DNA damage, during aging.
Screening the p53 status of human cell lines using a yeast functional assay
The results strongly support the previous findings that p53 inactivation is one of the most frequent genetic events that occurs during carcinogenesis and immortalization.
Angiogenic activity of osteopontin-derived peptide SVVYGLR.
Oxygen-dependent perturbation of life span and aging rate in the nematode.
Results show that changes in oxygen concentration perturb aging rate, and hence oxygen is involved in the specification of life span of the nematode.
Cytotoxicity of reactive oxygen species and related agents toward undifferentiated and differentiated rat phenochromocytoma PC12 cells.
The cytotoxicity of reactive oxygen species and related agents toward cultured rat adrenal medullary phenochromocytoma PC12 cells was examined and showed that the differentiated cells were more susceptible to these oxidative agents than the undifferentiated cells.
Oxidative injury of synapse and alteration of antioxidative defense systems in rats, and its prevention by vitamin E.
The results suggest that free radicals derived from oxygen may attack nerve terminals and peroxidize the plasma membrane, and support the idea that vitamin E contributes to the protection against nerve dysfunction caused by oxidative stress.