{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,12,2]],"date-time":"2025-12-02T15:22:25Z","timestamp":1764688945516},"reference-count":0,"publisher":"American Diabetes Association","issue":"8","content-domain":{"domain":["diabetesjournals.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[1997,8,1]]},"abstract":"<jats:p>Increasing evidence indicates that nitric oxide (NO) may play a role in immune-mediated injury to \u03b2-cells. One site for the action of this agent is the mitochondrion. Although the exact targets for damage within this organelle have yet to be fully elucidated, a potential location for injury is mitochondrial DNA (mtDNA). Therefore, experiments were initiated to evaluate damage to mtDNA caused by NO. Both exogenous NO generation (spermine\/NO adduct [sper\/NO]) and endogenous production of NO (IL-1\u03b2) were studied. To study the effects of exogenously produced NO, neonatal rat islet cells in monolayers were exposed to varying doses of sper\/NO for 30 min. Total cellular DNA was isolated and treated with alkali to produce strand breaks at abasic sites resulting from exposure to NO. Damage to mtDNA was evaluated using a quantitative Southern blot technique. The results showed that sper\/NO caused dose-dependent damage to mtDNA. Additionally, mtDNA was found to be more sensitive to injury generated by either source than a similarly sized fragment of nuclear DNA. To evaluate the effects of endogenously produced NO, \u03b2-cell cultures were treated with IL-1\u03b2 for 18 h. Other cultures were treated with IL-1\u03b2 and an inhibitor of the inducible form of nitric oxide synthase, aminoguanidine. DNA was evaluated as described for the sper\/NO studies. IL-1\u03b2 caused appreciable damage to mtDNA, and this damage was reduced in mtDNA from cultures treated with IL-1\u03b2 and aminoguanidine. These studies show that mtDNA is a sensitive target for NO generated both endogenously and exogenously and that this DNA is more vulnerable to NO-induced damage than nuclear DNA.<\/jats:p>","DOI":"10.2337\/diab.46.8.1291","type":"journal-article","created":{"date-parts":[[2013,9,19]],"date-time":"2013-09-19T17:42:54Z","timestamp":1379612574000},"page":"1291-1296","update-policy":"http:\/\/dx.doi.org\/10.2337\/ada-journal-policies","source":"Crossref","is-referenced-by-count":28,"title":["Mitochondrial DNA in \u03b2-Cells Is a Sensitive Target for Damage by Nitric Oxide"],"prefix":"10.2337","volume":"46","author":[{"given":"Glenn L","family":"Wilson","sequence":"first","affiliation":[{"name":"Department of Structural and Cellular Biology, The University of South Alabama,\u2008Mobile, Alabama."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Nancy J","family":"Patton","sequence":"additional","affiliation":[{"name":"Department of Structural and Cellular Biology, The University of South Alabama,\u2008Mobile, Alabama."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Susan P","family":"LeDoux","sequence":"additional","affiliation":[{"name":"Department of Structural and Cellular Biology, The University of South Alabama,\u2008Mobile, Alabama."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"1167","container-title":["Diabetes"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/journals.org\/diabetes\/diabetes\/article-pdf\/46\/8\/1291\/362680\/46-8-1291.pdf","content-type":"application\/pdf","content-version":"vor","intended-application":"syndication"},{"URL":"https:\/\/diabetesjournals.org\/diabetes\/article-pdf\/46\/8\/1291\/362680\/46-8-1291.pdf","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,11,2]],"date-time":"2022-11-02T16:34:00Z","timestamp":1667406840000},"score":1,"resource":{"primary":{"URL":"https:\/\/diabetesjournals.org\/diabetes\/article\/46\/8\/1291\/9282\/Mitochondrial-DNA-in-Cells-Is-a-Sensitive-Target"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1997,8,1]]},"references-count":0,"journal-issue":{"issue":"8","published-print":{"date-parts":[[1997,8,1]]}},"URL":"https:\/\/doi.org\/10.2337\/diab.46.8.1291","relation":{},"ISSN":["0012-1797","1939-327X"],"issn-type":[{"value":"0012-1797","type":"print"},{"value":"1939-327X","type":"electronic"}],"subject":[],"published":{"date-parts":[[1997,8,1]]}}}