Bisphenol　A　(BPA)　is　a　well-known　endocrine-disrupting　chemical　that　is　ubiquitously　present　in　the　environment.　In　the　present　study,　4-h　post-fertilization　(hpf)　zebrafish　embryos　were　exposed　to　various　environmentally　relevant　concentrations　of　BPA　(0.1,　1,　10,　100,　and　1000　mu　g/L)　until　72　and　168　hpf,　and　the　accumulation　pattern　of　BPA　and　its　potential　to　induce　toxicity　through　apoptosis　were　determined.　Compared　to　BPA　concentrations　in　larvae　at　168　hpf,　BPA　concentrations　in　embryos　exposed　until　72　hpf　were　at　relatively　higher　levels　(p　＜　0.05)　with　higher　bioconcentration　factor　(BCF)　values.　The　nonlinear　fitting　analysis　indicated　that　the　BCF　values　of　BPA　in　fish　embryos/larvae　were　significantly　correlated　to　the　log　10-transformed　BPA　exposure　concentrations　in　water　in　an　inverse　concentration-dependent　manner.　Fish　accumulated　more　BPA　as　the　exposure　concentrations　increased;　however,　their　accumulation　capacity　of　BPA　declined　and　tended　to　be　saturated　in　the　high　exposure　groups　of　BPA.　Moreover,　caspase-3　activity　was　significantly　induced　upon　BPA　exposure　at　0.1,　1,　10,　and　100　mu　g/L　BPA　at　72　hpf,　and　also　at　10　and　100　mu　g/L　BPA　at　168　hpf.　Correspondingly,　exposure　to　10　and　100　mu　g/L　of　BPA　significantly　increased　the　DNA　fragmentation　in　the　extracted　DNA　at　168　hpf　as　determined　by　DNA　ladder　analysis.　In　addition,　the　expression　patterns　of　four　genes　related　to　apoptosis　including　caspase-3,　bax,　p53,　and　c-jun　were　significantly　up-regulated　(p　＜　0.05)　in　fish　embryos/larvae　upon　BPA　exposure　at　72　and　168　hpf.　Our　results　revealed　that　low　and　environmentally　relevant　concentrations　of　BPA　could　be　significantly　accumulated　in　zebrafish　and　induced　apoptosis　with　involvement　of　the　regulation　of　caspase-3　and　other　apoptosis-related　genes.