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10.1080/07315724.2006.10719547 http://scihub22266oqcxt.onion/10.1080/07315724.2006.10719547 17031004!ä!17031004 Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=17031004&cmd=llinks): Failed to open stream: HTTP request failed! 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N-acetylcysteine partially reverses oxidative stress and apoptosis exacerbated by Mg-deficiency culturing conditions in primary cultures of rat and human hepatocytes |pdf=|usr=}}{{17031004}} gab.com Text N-acetylcysteine partially reverses oxidative stress and apoptosis exacerbated by Mg-deficiency culturing conditions in primary cultures of rat and human hepatocytes JO: J Am Coll Nutr http://www.kidney.de/pget.php?&tw=1&pmid=17031004 #FOAvip OBJECTIVE: The effects of magnesium (Mg) deficiency on the rate of oxidative stress and apoptosis in primary cultures of human hepatocytes were compared to cultured rat hepatocytes. The possible reversion by N-acetylcysteine (NAC) in Mg-deficient culturing conditions was evaluated. METHODS: Incubations were conducted for up to 72 h in media containing a deficient (0-0.4 mM) or a physiological (0.8 mM) Mg concentration, and in the presence or absence of NAC after 24 h of culture in these Mg concentration conditions. RESULTS: We obtained similar profiles in terms of apoptosis and oxidative stress in primary cultures of human hepatocytes, as compared to rat hepatocytes, i.e. a Mg concentration-dependent effect on the caspase-3 activity and GSH levels after 72 h of culture, caspase-3 activity being highest and GSH levels being lowest in Mg-free cultures. The addition of NAC to culture media after the first 24 h of culture increased GSH concentrations. This was accompanied in Mg-deficient cultures by a decrease in both the caspase-3 activity and the lipid peroxidation. However, when culturing hepatocytes with physiological Mg concentrations, an increase in both caspase-3 activity and lipid peroxidation was observed. CONCLUSIONS: Our results indicate that Mg deficiency exacerbates the rate of apoptosis in cultured hepatocytes, associated with an increase in oxidative stress, the sensitivity of human hepatocytes being equivalent to that of rat hepatocytes. They also indicate a dual role of NAC and/or GSH, i.e. protective for hepatocytes placed in a Mg-deficient environment, while deleterious for hepatocytes placed in a Mg-physiological environment. Twit Text FOAVip N-acetylcysteine partially reverses oxidative stress and apoptosis exacerbated by Mg-deficiency culturing conditions in primary cultures of rat and human hepatocytes ????J Am Coll Nutr http://www.kidney.de/pget.php?&tw=1&pmid=17031004 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=17031004 #FOAvip English Wikipedia <ref>{{Cite pmid|17031004}}</ref> N-acetylcysteine partially reverses oxidative stress and apoptosis exacerbated by Mg-deficiency culturing conditions in primary cultures of rat and human hepatocytes #MMPMID17031004 Martin H; Abadie C; Heyd B; Mantion G; Richert L; Berthelot A J Am Coll Nutr 2006[Oct]; 25 (5): 363-9 PMID17031004show ga OBJECTIVE: The effects of magnesium (Mg) deficiency on the rate of oxidative stress and apoptosis in primary cultures of human hepatocytes were compared to cultured rat hepatocytes. The possible reversion by N-acetylcysteine (NAC) in Mg-deficient culturing conditions was evaluated. METHODS: Incubations were conducted for up to 72 h in media containing a deficient (0-0.4 mM) or a physiological (0.8 mM) Mg concentration, and in the presence or absence of NAC after 24 h of culture in these Mg concentration conditions. RESULTS: We obtained similar profiles in terms of apoptosis and oxidative stress in primary cultures of human hepatocytes, as compared to rat hepatocytes, i.e. a Mg concentration-dependent effect on the caspase-3 activity and GSH levels after 72 h of culture, caspase-3 activity being highest and GSH levels being lowest in Mg-free cultures. The addition of NAC to culture media after the first 24 h of culture increased GSH concentrations. This was accompanied in Mg-deficient cultures by a decrease in both the caspase-3 activity and the lipid peroxidation. However, when culturing hepatocytes with physiological Mg concentrations, an increase in both caspase-3 activity and lipid peroxidation was observed. CONCLUSIONS: Our results indicate that Mg deficiency exacerbates the rate of apoptosis in cultured hepatocytes, associated with an increase in oxidative stress, the sensitivity of human hepatocytes being equivalent to that of rat hepatocytes. They also indicate a dual role of NAC and/or GSH, i.e. protective for hepatocytes placed in a Mg-deficient environment, while deleterious for hepatocytes placed in a Mg-physiological environment. |Acetylcysteine/*pharmacology[MESH] |Animals[MESH] |Apoptosis/*drug effects[MESH] |Caspase 3/metabolism[MESH] |Cells, Cultured[MESH] |Dose-Response Relationship, Drug[MESH] |Free Radical Scavengers/pharmacology[MESH] |Glutathione/metabolism[MESH] |Hepatocytes/cytology/*physiology[MESH] |Humans[MESH] |Lipid Peroxidation/drug effects[MESH] |Magnesium Deficiency/*physiopathology[MESH] |Magnesium/metabolism/*pharmacology[MESH] |Oxidative Stress/*drug effects[MESH]N-acetylcysteine partially reverses oxidative stress and apoptosis exa(epmc).pdf DeepDyve Pubget Overpricing