HEALTH NEWS
Study Title:
Prooxidative toxicity and selenoprotein suppression by cerivastatin in muscle cells.
Study Abstract
Statins are the most widely used drugs for the treatment of hypercholesterolemia. In spite of their overall favorable safety profile, they do possess serious myotoxic potential, whose molecular origin has remained equivocal. Here, we demonstrate in cultivated myoblasts and skeletal muscle cells that cerivastatin at nanomolar concentrations interferes with selenoprotein synthesis and evokes a heightened vulnerability of the cells toward oxidative stressors. A correspondingly increased vulnerability was found with atorvastatin, albeit at higher concentrations than with cerivastatin. In selenium-saturated cells, cerivastatin caused a largely indiscriminate suppression of selenoprotein biosynthesis and reduced the steady state-levels of glutathione peroxidase 1 (GPx1) and selenoprotein N (SelN). Selenite, ebselen, and ubiquinone were unable to prevent the devitalizing effect of statin treatment, despite the fact that the cellular baseline resistance against tert-butyl hydroperoxide was significantly increased by picomolar sodium selenite. Mevalonic acid, in contrast, entirely prevented the statin-induced decrease in peroxide resistance. These results indicate that muscle cells may be particularly susceptible to a statin-induced suppression of essential antioxidant selenoproteins, which provides an explanation for the disposition of these drugs to evoke adverse muscular side-effects.
Study Information
Toxicol Lett. 2012 Dec 17;215(3):219-27. doi: 10.1016/j.toxlet.2012.10.010. Epub 2012 Oct 22. PMID: 23092657.Full Study
https://pubmed.ncbi.nlm.nih.gov/23092657/Recent News
Arabinogalactan Boosts Lymph Flow and Immunity
Protect Your Gut Mucosal Barrier for Immune Health and Vitality
The Truth About Sugar Substitutes: Are Stevia, Sucralose, and Saccharin Safe?
Boost Your Digestive Power for Better Nutrient Absorption and Gut Health
MTHFR Gene and The Importance of Methyl B12 and Methyl Folate