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This study is designed to determine whether\n                      <jats:styled-content style=\"fixed-case\">D<\/jats:styled-content>\n                      \u2010\n                      <jats:styled-content style=\"fixed-case\">L<\/jats:styled-content>\n                      \u2010\n                      <jats:styled-content style=\"fixed-case\">s<\/jats:styled-content>\n                      ulforaphane (\n                      <jats:styled-content style=\"fixed-case\">SFN<\/jats:styled-content>\n                      ) can protect neural crest cells (\n                      <jats:styled-content style=\"fixed-case\">NCCs<\/jats:styled-content>\n                      ), an ethanol\u2010sensitive cell population implicated in fetal alcohol spectrum disorders, against ethanol\u2010induced apoptosis and whether protective effects of\n                      <jats:styled-content style=\"fixed-case\">SFN<\/jats:styled-content>\n                      are mediated by the induction of\n                      <jats:styled-content style=\"fixed-case\">N<\/jats:styled-content>\n                      rf2\u2010mediated antioxidant response.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Experimental Approach<\/jats:title>\n                    <jats:p>\n                      Control,\n                      <jats:styled-content style=\"fixed-case\">SFN<\/jats:styled-content>\n                      \u2010treated or\n                      <jats:styled-content style=\"fixed-case\">N<\/jats:styled-content>\n                      rf2\u2010\n                      <jats:styled-content style=\"fixed-case\">siRNA<\/jats:styled-content>\n                      transfected\n                      <jats:styled-content style=\"fixed-case\">NCCs<\/jats:styled-content>\n                      were exposed to ethanol.\n                      <jats:styled-content style=\"fixed-case\">N<\/jats:styled-content>\n                      rf2 activation, the expression and activities of\n                      <jats:styled-content style=\"fixed-case\">N<\/jats:styled-content>\n                      rf2 downstream antioxidant proteins, reactive oxygen species generation and apoptosis were determined in control and ethanol\u2010exposed\n                      <jats:styled-content style=\"fixed-case\">NCCs<\/jats:styled-content>\n                      .\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Key Results<\/jats:title>\n                    <jats:p>\n                      Exposure of\n                      <jats:styled-content style=\"fixed-case\">NCCs<\/jats:styled-content>\n                      to\n                      <jats:styled-content style=\"fixed-case\">SFN<\/jats:styled-content>\n                      alone significantly increased\n                      <jats:styled-content style=\"fixed-case\">N<\/jats:styled-content>\n                      rf2 activation and the expression of\n                      <jats:styled-content style=\"fixed-case\">N<\/jats:styled-content>\n                      rf2 downstream antioxidants as well as the activities of the antioxidant enzymes. Treatment of\n                      <jats:styled-content style=\"fixed-case\">NCCs<\/jats:styled-content>\n                      with\n                      <jats:styled-content style=\"fixed-case\">SFN<\/jats:styled-content>\n                      along with ethanol significantly decreased ethanol\u2010induced oxidative stress and apoptosis. In contrast, knockdown of\n                      <jats:styled-content style=\"fixed-case\">N<\/jats:styled-content>\n                      rf2 by\n                      <jats:styled-content style=\"fixed-case\">siRNA<\/jats:styled-content>\n                      significantly increased the sensitivity of\n                      <jats:styled-content style=\"fixed-case\">NCCs<\/jats:styled-content>\n                      to ethanol\u2010induced oxidative stress and apoptosis. Suppression of\n                      <jats:styled-content style=\"fixed-case\">N<\/jats:styled-content>\n                      rf2 signalling in\n                      <jats:styled-content style=\"fixed-case\">NCCs<\/jats:styled-content>\n                      also significantly diminished\n                      <jats:styled-content style=\"fixed-case\">SFN<\/jats:styled-content>\n                      \u2010mediated antioxidant response and abolished the protective effects of\n                      <jats:styled-content style=\"fixed-case\">SFN<\/jats:styled-content>\n                      on ethanol\u2010induced oxidative stress and apoptosis.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions and Implications<\/jats:title>\n                    <jats:p>\n                      These results demonstrated that\n                      <jats:styled-content style=\"fixed-case\">N<\/jats:styled-content>\n                      rf2\u2010mediated antioxidant response plays an important role in the susceptibility of\n                      <jats:styled-content style=\"fixed-case\">NCCs<\/jats:styled-content>\n                      to ethanol\u2010induced oxidative stress and apoptosis and that the protection of\n                      <jats:styled-content style=\"fixed-case\">SFN<\/jats:styled-content>\n                      against ethanol\u2010induced oxidative stress and apoptosis in\n                      <jats:styled-content style=\"fixed-case\">NCCs<\/jats:styled-content>\n                      is mediated by the induction of\n                      <jats:styled-content style=\"fixed-case\">N<\/jats:styled-content>\n                      rf2 signalling.\n                    <\/jats:p>\n                  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