![]() In addition, DUOX was significantly downregulated in pancreatic cancer specimens compared with normal pancreas tissues. An inducible catalase system, to test causality for the role of hydrogen peroxide, reversed the P-AscH −–induced increases in DUOX, whereas DUOX inhibition partially rescued P-AscH −–induced toxicity. Sources for this increase in ROS and OCR were DUOX 1 and 2, which are silenced in pancreatic ductal adenocarcinoma, but upregulated with P-AscH − treatment. P-AscH − resulted in sustained increases in the rate of cellular oxygen consumption (OCR) and reactive oxygen species (ROS) in tumor cells, with no changes in nontumorigenic cells. Cellular bioenergetic profiling following treatment with P-AscH − was examined in tumorigenic and nontumorigenic cells. ![]() ![]() This study examines whether an increase in hydrogen peroxide is sustained posttreatment and potential mechanisms involved in this process. Pharmacologic ascorbate treatment (P-AscH −, high-dose, intravenous vitamin C) results in a transient short-term increase in the flux of hydrogen peroxide that is preferentially cytotoxic to cancer cells versus normal cells. ![]()
0 Comments
Leave a Reply. |
AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |