Electric Literature of 2043-57-4, The transformation of simple hydrocarbons into more complex and valuable products via catalytic C¨CH bond functionalisation has revolutionised modern synthetic chemistry. 2043-57-4, Name is 1,1,1,2,2,3,3,4,4,5,5,6,6-Tridecafluoro-8-iodooctane, SMILES is ICCC(F)(F)C(F)(F)C(F)(F)C(F)(F)C(F)(F)C(F)(F)F, belongs to iodides-buliding-blocks compound. In a article, author is Vitale, M, introduce new discover of the category.
Iodide excess induces apoptosis in thyroid cells through a p53-independent mechanism involving oxidative stress
Thyroid toxicity of iodide excess has been demonstrated in animals fed with an iodide-rich diet; in vitro iodide is cytotoxic, inhibits cell growth, and induces morphological changes in thyroid cells of some species. In this study, we investigated the effect of iodide excess in an immortalized thyroid cell line (TAD-2) in primary cultures of human thyroid cells and in cells of nonthyroid origin. Iodide displayed a dose-dependent cytotoxicity in both TAD-2 and primary thyroid cells, although at different concentrations, whereas it had no effect on cells of nonthyroid origin. Thyroid cells treated with iodide excess underwent apoptosis, as evidenced by morphological changes, plasma membrane phosphatidylserine exposure, and DNA fragmentation. Apoptosis was unaffected by protein synthesis inhibition, whereas inhibition of peroxidase enzymatic activity by Dropylthiouracil completely blocked iodide cytotoxicity. During KI treatment, reactive oxygen species were produced, and lipid peroxide levels increased markedly. Inhibition of endogenous p53 activity did not affect the sensitivity of TAD-2 cells to iodide, and Western blot analysis demonstrated that p53, Bcl-2, Bcl-XL, and Bar protein expression did not change when cells were treated with iodide. These data indicate that excess molecular iodide, generated by oxidation of ionic iodine by endogenous peroxidases, induces apoptosis in thyroid cells through a mechanism involving generation of free radicals. This type of apoptosis is p53 independent, does not require protein synthesis, and is not induced by modulation of Bcl-2, Bcl-XL, or Bar protein expression.
Electric Literature of 2043-57-4, The reactant in an enzyme-catalyzed reaction is called a substrate. Enzyme inhibitors cause a decrease in the reaction rate of an enzyme-catalyzed reaction.I hope my blog about 2043-57-4 is helpful to your research.