@prefix dcat: <http://www.w3.org/ns/dcat#> .
@prefix dct: <http://purl.org/dc/terms/> .
@prefix foaf: <http://xmlns.com/foaf/0.1/> .
@prefix vcard: <http://www.w3.org/2006/vcard/ns#> .
@prefix xsd: <http://www.w3.org/2001/XMLSchema#> .

<https://rec.harvest-normandie.data4citizen.com/dataset/oai-hal-hal-00098647v1> a dcat:Dataset ;
    dct:description """
              Glutathione depletion either decreased or increased death-receptor-mediated apoptosis in previous studies. Comparison of the durations of glutathione depletion before death-receptor stimulation in these studies might suggest a different effect of prolonged versus acute thiol depletion. We compared the effects of the prolonged glutathione depletion caused by a sulfur amino acid-deficient (SAA(-)) diet and the acute depletion caused by a single dose of phorone on hepatic apoptosis triggered by the administration of an agonistic anti-Fas antibody. The chronic SAA(-) diet did not affect hepatic Fas or Bcl-XL, but increased p53 and Bax, and exacerbated Fas-mediated mitochondrial membrane depolarization, electron-microscopy-proven outer mitochondrial membrane rupture, cytochrome c translocation to the cytosol, and caspase 3 activation. These effects were prevented by cyclosporin A, an inhibitor of mitochondrial permeability transition. The SAA(-) diet increased internucleosomal DNA fragmentation, the percentage of apoptotic hepatocytes, serum alanine transaminase (ALT) activity, and mortality after Fas stimulation. Despite a similar decrease in hepatic glutathione, administration of a single dose of phorone 1 hour before the anti-Fas antibody did not change p53 or Bax, and did not enhance Fas-induced mitochondrial permeability transition and toxicity. However, 4 repeated doses of phorone (causing more prolonged glutathione depletion) increased Bax and Fas-mediated toxicity. In conclusion, a chronic SAA(-) diet, but not acute phorone administration, increases p53 and Bax, and enhances Fas-induced mitochondrial permeability transition and apoptosis. Thiol depletion could cause oxidative stress that requires several hours to increase p53; the latter induces Bax, which translocates to mitochondria after Fas stimulation.
            """ ;
    dct:identifier "hal-00098647" ;
    dct:issued "2026-05-05T12:20:34.046569"^^xsd:dateTime ;
    dct:language "en" ;
    dct:modified "2026-05-05T12:20:34.046573"^^xsd:dateTime ;
    dct:publisher <https://rec.harvest-normandie.data4citizen.com/organization/cce9db95-46d9-4dc2-84b6-764215d0a002> ;
    dct:title "Prolonged, but not acute, glutathione depletion promotes Fas-mediated mitochondrial permeability transition and apoptosis in mice." ;
    dcat:contactPoint [ a vcard:Organization ;
            vcard:fn "CCSD" ] ;
    dcat:distribution <https://rec.harvest-normandie.data4citizen.com/dataset/oai-hal-hal-00098647v1/resource/3fbb3f77-e36a-40a9-a66e-327d33dc36d6> ;
    dcat:keyword "apoptosis",
        "bax",
        "fas",
        "glutathione",
        "infoeu-reposemanticsarticle",
        "journal-articles",
        "mitochondrial-permeability-transition",
        "p53",
        "sdvsppharmalife-sciences-q-biopharmaceutical-sciencespharmacology" ;
    dcat:landingPage <ISSN:%200270-9139> .

<ISSN:%200270-9139> a foaf:Document .

<https://rec.harvest-normandie.data4citizen.com/dataset/oai-hal-hal-00098647v1/resource/3fbb3f77-e36a-40a9-a66e-327d33dc36d6> a dcat:Distribution ;
    dct:format "HTML" ;
    dct:issued "2026-05-05T12:20:34.054127"^^xsd:dateTime ;
    dct:modified "2026-05-05T12:20:34.030626"^^xsd:dateTime ;
    dct:title "Prolonged, but not acute, glutathione depletion promotes Fas-mediated mitochondrial permeability transition and apoptosis in mice." ;
    dcat:accessURL <https://hal.science/hal-00098647> .

<https://rec.harvest-normandie.data4citizen.com/organization/cce9db95-46d9-4dc2-84b6-764215d0a002> a foaf:Agent ;
    foaf:name "test_moissonnage_selune" .