{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,9]],"date-time":"2026-10-09T11:34:05Z","timestamp":1791545645603,"version":"4.3.4"},"reference-count":40,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2011,7,22]],"date-time":"2011-07-22T00:00:00Z","timestamp":1311292800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Environmental Toxicology"],"published-print":{"date-parts":[[2013,6]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>The mechanisms underlying the neurotoxicology of endemic fluorosis still remain obscure. To explore lactate dehydrogenase (LDH) leakage, intracellular Ca<jats:sup>2+<\/jats:sup> concentration ([Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>) and reactive oxygen species (ROS) production induced by fluoride, human neuroblastoma (SH\u2010SY5Y) cells were incubated with sodium fluoride (NaF, 20, 40, 80 mg\/L) for 24 h, with 40 mg\/L NaF for 3, 6, 12, 18, 24 h, and <jats:italic>N<\/jats:italic>\u2010acetyl\u2010<jats:sc>L<\/jats:sc>\u2010cysteine (NAC), ethyleneglycol\u2010bis\u2010(\u03b2\u2010aminoethyl ether)\u2010<jats:italic>N<\/jats:italic>,<jats:italic>N<\/jats:italic>,<jats:italic>N<\/jats:italic>\u2032,<jats:italic>N<\/jats:italic>\u2032\u2010tetraacetic acid (EGTA), 1,2\u2010bis(<jats:italic>O<\/jats:italic>\u2010aminophenoxy)ethane\u2010<jats:italic>N<\/jats:italic>,<jats:italic>N<\/jats:italic>,<jats:italic>N<\/jats:italic>\u2032,<jats:italic>N<\/jats:italic>\u2032\u2010tetraacetic acid tetra(acetoxymethyl) ester (BAPTA\u2010AM) alone or combined with fluoride (40 mg\/L) respectively for 12 h <jats:italic>in vitro<\/jats:italic>. The results showed that the LDH levels in the 40 and 80 mg\/L fluoride\u2010treated groups were significantly higher than that of the control group (in the test level of 0.05, the difference were statistical significance). [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub> and ROS reached a peak at 3 h and 12 h respectively after exposure to 40 mg\/L fluoride. Fluoride coincubated with NAC (antioxidant) dramatically decreased ROS and LDH levels compared with the fluoride only group (in the test level of 0.05, the difference were statistical significance). However, fluoride\u2010induced increase in [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub> was not affected by NAC. BAPTA\u2010AM (intracellular calcium chelator) markedly lowered fluoride\u2010induced increase of [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>, ROS and LDH levels while EGTA (extracellular calcium chelator) have no effects on them. These results indicate that fluoride\u2010related Ca<jats:sup>2+<\/jats:sup> release from the site of intracellular calcium storage causes the elevation of ROS contributing to the cytotoxicity in SH\u2010SY5Y cells. \u00a9 2011 Wiley Periodicals, Inc. Environ Toxicol, 2013.<\/jats:p>","DOI":"10.1002\/tox.20721","type":"journal-article","created":{"date-parts":[[2011,7,24]],"date-time":"2011-07-24T17:53:35Z","timestamp":1311530015000},"page":"307-312","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":25,"title":["Relationship between intracellular Ca<sup>2+<\/sup> and ROS during fluoride\u2010induced injury in SH\u2010SY5Y 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