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We began analyzing https://link.springer.com/article/10.1007/s10495-011-0633-x, but it redirected us to https://link.springer.com/article/10.1007/s10495-011-0633-x. The analysis below is for the second page.

Title[redir]:
Deoxycholic and chenodeoxycholic bile acids induce apoptosis via oxidative stress in human colon adenocarcinoma cells | Apoptosis
Description:
The continuous exposure of the colonic epithelium to high concentrations of bile acids may exert cytotoxic effects and has been related to pathogenesis of colon cancer. A better knowledge of the mechanisms by which bile acids induce toxicity is still required and may be useful for the development of new therapeutic strategies. We have studied the effect of deoxycholic acid (DCA) and chenodeoxycholic acid (CDCA) treatments in BCS-TC2 human colon adenocarcinoma cells. Both bile acids promote cell death, being this effect higher for CDCA. Apoptosis is detected after 30 min–2 h of treatment, as observed by cell detachment, loss of membrane asymmetry, internucleosomal DNA degradation, appearance of mitochondrial transition permeability (MPT), and caspase and Bax activation. At longer treatment times, apoptosis is followed in vitro by secondary necrosis due to impaired mitochondrial activity and ATP depletion. Bile acid-induced apoptosis is a result of oxidative stress with increased ROS generation mainly by activation of plasma membrane enzymes, such as NAD(P)H oxidases and, to a lower extent, PLA2. These effects lead to a loss of mitochondrial potential and release of pro-apoptotic factors to the cytosol, which is confirmed by activation of caspase-9 and -3, but not caspase-8. This initial apoptotic steps promote cleavage of Bcl-2, allowing Bax activation and formation of additional pores in the mitochondrial membrane that amplify the apoptotic signal.

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Keywords {🔍}

article, google, scholar, pubmed, cas, bile, apoptosis, acid, colon, cells, acids, cell, human, olmo, adenocarcinoma, turnay, mitochondrial, biol, cancer, membrane, chem, lizarbe, caspase, activation, deoxycholic, stress, permeability, res, induces, privacy, cookies, content, oxidative, lecona, effect, transition, acidinduced, access, butyrate, biochem, protection, publish, search, chenodeoxycholic, induce, barrasa, pérezramos, death, release, apoptotic,

Topics {✒️}

12α-trihydroxy-5β-cholanoic acid 12α-dihydroxy-5β-cholanoic acid 7β-dihydroxy-5β-cholanoic acid bile-acid-induced cell injury reactive oxygen species 7α-dihydroxy-5β-cholanoic acid 3α-hydroxy-5β-cholanic acid month download article/chapter bile acid-induced apoptosis bile salt-induced apoptosis glycochenodeoxycholic acid-induced apoptosis triton x-100-induced apoptosis cd95-dependent hepatocyte apoptosis n-acetyl-cysteine parp lópez de silanes bile acid hydrophobicity biliary epithelial cells protein kinase ceta tumour colon cells src family kinases article apoptosis aims emilio lecona full article pdf colon cancer hydrophobic bile acids bile acids modulate privacy choices/manage cookies caco-2 cell line author information authors pablo pérez-ramos human gastrointestinal cancers intestinal disease bcl-2 promotes release colonic epithelial cells cell death caspase-3-dependent cleavage gonzález de buitrago sk-hep-1 cells check access instant access bile salts bile acid annexin a1 expression mitochondrial transition permeability mitochondrial permeability transition article barrasa cancer res 64 bcs-tc2 plasma membrane enzymes bile acids

Schema {🗺️}

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         description:The continuous exposure of the colonic epithelium to high concentrations of bile acids may exert cytotoxic effects and has been related to pathogenesis of colon cancer. A better knowledge of the mechanisms by which bile acids induce toxicity is still required and may be useful for the development of new therapeutic strategies. We have studied the effect of deoxycholic acid (DCA) and chenodeoxycholic acid (CDCA) treatments in BCS-TC2 human colon adenocarcinoma cells. Both bile acids promote cell death, being this effect higher for CDCA. Apoptosis is detected after 30 min–2 h of treatment, as observed by cell detachment, loss of membrane asymmetry, internucleosomal DNA degradation, appearance of mitochondrial transition permeability (MPT), and caspase and Bax activation. At longer treatment times, apoptosis is followed in vitro by secondary necrosis due to impaired mitochondrial activity and ATP depletion. Bile acid-induced apoptosis is a result of oxidative stress with increased ROS generation mainly by activation of plasma membrane enzymes, such as NAD(P)H oxidases and, to a lower extent, PLA2. These effects lead to a loss of mitochondrial potential and release of pro-apoptotic factors to the cytosol, which is confirmed by activation of caspase-9 and -3, but not caspase-8. This initial apoptotic steps promote cleavage of Bcl-2, allowing Bax activation and formation of additional pores in the mitochondrial membrane that amplify the apoptotic signal.
         datePublished:2011-07-23T00:00:00Z
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      headline:Deoxycholic and chenodeoxycholic bile acids induce apoptosis via oxidative stress in human colon adenocarcinoma cells
      description:The continuous exposure of the colonic epithelium to high concentrations of bile acids may exert cytotoxic effects and has been related to pathogenesis of colon cancer. A better knowledge of the mechanisms by which bile acids induce toxicity is still required and may be useful for the development of new therapeutic strategies. We have studied the effect of deoxycholic acid (DCA) and chenodeoxycholic acid (CDCA) treatments in BCS-TC2 human colon adenocarcinoma cells. Both bile acids promote cell death, being this effect higher for CDCA. Apoptosis is detected after 30 min–2 h of treatment, as observed by cell detachment, loss of membrane asymmetry, internucleosomal DNA degradation, appearance of mitochondrial transition permeability (MPT), and caspase and Bax activation. At longer treatment times, apoptosis is followed in vitro by secondary necrosis due to impaired mitochondrial activity and ATP depletion. Bile acid-induced apoptosis is a result of oxidative stress with increased ROS generation mainly by activation of plasma membrane enzymes, such as NAD(P)H oxidases and, to a lower extent, PLA2. These effects lead to a loss of mitochondrial potential and release of pro-apoptotic factors to the cytosol, which is confirmed by activation of caspase-9 and -3, but not caspase-8. This initial apoptotic steps promote cleavage of Bcl-2, allowing Bax activation and formation of additional pores in the mitochondrial membrane that amplify the apoptotic signal.
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