{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T03:30:12Z","timestamp":1787023812192,"version":"build-2736575974"},"reference-count":30,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2010,9,1]],"date-time":"2010-09-01T00:00:00Z","timestamp":1283299200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Periodontology"],"published-print":{"date-parts":[[2010,9]]},"abstract":"<jats:p>\n                    <jats:bold>Background:<\/jats:bold>\n                    It is well known that hydrogen sulfide (H\n                    <jats:sub>2<\/jats:sub>\n                    S), the main substance causing physiologic halitosis, is also involved in the etiology of periodontitis. Gingival crevicular epithelium is the first barrier against periodontal pathogens and their products; keratinocyte stem cells play key roles in maintaining this barrier. An increased apoptotic process can affect keratinocyte stem cells, having a direct impact on oral epithelial tissue architecture. Our objective is to determine whether H\n                    <jats:sub>2<\/jats:sub>\n                    S induces apoptosis in human keratinocyte stem cells.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Methods:<\/jats:bold>\n                    Apoptosis levels; p53 activity; reactive oxygen species; mitochondrial membrane depolarization; cytochrome C release; and caspase\u20109, \u20108, and \u20103 were assessed using enzyme\u2010linked immunosorbent assay and flow cytometry. Genomic DNA damage was examined using single\u2010cell gel electrophoresis. Real\u2010time polymerase chain reaction was used for Bax detection.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Results:<\/jats:bold>\n                    The percentage of apoptotic cells was significantly increased (20.5% \u00b1 1.6% versus 4.5% \u00b1 1.1% at 24 hours and 37.8% \u00b1 5.4% versus 4.8% \u00b1 0.9% at 48 hours;\n                    <jats:italic>P &lt;<\/jats:italic>\n                    0.05, respectively; n = 5). Mitochondrial membrane potential was collapsed and reactive oxygen species levels were significantly increased compared to their control groups. At each time point the amount of released cytochrome C into the cytosol was significantly increased. Caspase\u20109 and \u20103 activities were significantly increased (\n                    <jats:italic>P<\/jats:italic>\n                    &lt;0.05), whereas caspase\u20108 remained inactive. After both 24 and 48 hours, total and phosphorylated p53 levels were significantly increased.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Conclusion:<\/jats:bold>\n                    We conclude that H\n                    <jats:sub>2<\/jats:sub>\n                    S can induce apoptosis in human keratinocyte stem cells, a key component of the epithelial barrier, following DNA damage and p53 activation.\n                  <\/jats:p>","DOI":"10.1902\/jop.2010.100080","type":"journal-article","created":{"date-parts":[[2010,5,17]],"date-time":"2010-05-17T12:36:38Z","timestamp":1274099798000},"page":"1317-1323","source":"Crossref","is-referenced-by-count":29,"title":["Oral Malodorous Compound Causes Oxidative Stress and p53\u2010Mediated Programmed Cell Death in Keratinocyte Stem Cells"],"prefix":"10.1002","volume":"81","author":[{"given":"Bogdan","family":"Calenic","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ken","family":"Yaegaki","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ana","family":"Kozhuharova","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Toshio","family":"Imai","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2010,9]]},"reference":[{"key":"e_1_2_7_2_1","doi-asserted-by":"publisher","DOI":"10.1016\/0003-9969(71)90062-8"},{"key":"e_1_2_7_3_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-0765.1992.tb01673.x"},{"key":"e_1_2_7_4_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.jdsr.2008.06.003"},{"key":"e_1_2_7_5_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-0765.2007.00999.x"},{"key":"e_1_2_7_6_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-0765.1992.tb01736.x"},{"key":"e_1_2_7_7_1","first-page":"87","volume-title":"Bad 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