Indomethacin-induced mitochondrial dysfunction and oxidative stress in villus enterocytes

摘要: Nonsteroidal anti-inflammatory drugs (NSAIDs) are known to cause small intestinal damage but the pathogenesis of this toxicity is not well established. Intestinal epithelial cells thought be affected by these in course their absorption. These different types, viz. villus, middle and crypt cells. There little information on which cells, if any, particularly vulnerable effects NSAIDs. This paper aimed study indomethacin, an NSAID commonly used studies, populations enterocytes. Effects drug were assessed terms oxidative damage, mitotic activity, mitochondrial function lipid composition enterocytes isolated from intestine rats that had been orally administered indomethacin. In addition, arginine zinc protecting against such changes assessed. Cell viability, tetrazolium dye (MTT) reduction oxygen uptake significantly reduced villus tip dosed with drug. Thymidine was higher cell fraction rats. Similarly, products peroxidation elevated a corresponding decrease level anti-oxidant, alpha-tocopherol. preparations various enterocyte fractions, significant functional impairment altered seen mainly mitochondria Arginine pre-treatment found protect effects. results suggest for first time more damaging indomethacin stress possibly involved damage.