| External factors: | Selenium Compounds |
| Aging type: | Accelerate |
| Aging characteristic: |
| Category: | Chemical compounds |
| Phenotype: | Cancer |
| Experiment: | SA-β-gal activity assay//BrdU Assay |
| Description: | The selenium treatment resulted in the expression of SA-β-galactosidase in the non-cancerous MRC-5 and CRL-1790 cells in a dose-dependent manner from a concentration as low as 0.1 uM(Na2SeO3or MSeA) and 5 uM (MSeC). Strikingly, there was no detectable SA-β-galactosidase in the cancerous PC-3 and HCT 116 cells treated with selenium at doses that result in the majority of the MRC-5 cells senescing or even higher doses.Compared with the MRC-5 cells without selenium treatment, cellular exposure to Na2SeO3, MSeA, and MSeC resulted in a 4-,6.6-, and 2.3-fold reduction in BrdUrd incorporation, respectively. |
| Target gene: | ATM |
| R-EF-Target gene: | -- |
| Official symbol(s): | ATM |
| Target gene experiment: | SA-β-gal activity assay//Immunofluorescence |
| Target gene description: | Results from the SA-β-galactosidase analysis demonstrated that inhibition of ATM kinase activity prevented senescence induction in MRC-5 cells exposed to Na2SeO3(1uM), MSeA (1uM), or MSeC (50uM). Treatment of MRC-5 cells with anti-oxidants, NAC (a H2O2scavenger) and Tempo (a superoxide dismutase mimic), significantly suppressed senescence in MRC-5 cells treated with the selenium compounds.Tempo is more potent than NAC in the attenuation of senescence induced by Na2SeO3and MSeA. ROS contribute to the selenium-induced DNA damage response because the pATM Ser-1981 focus formation. |
| Regulatory pathway: | -- |
| R-EF-Pathway: | -- |
| Pathway experiment: | -- |
| Pathway description: | -- |
Annotation: