Heavy metal contamination of water body has become a serious threat to aquatic life forms specially to fish. Hexavalent chromium (Cr [VI]) is one of the most potent heavy metal toxicant. It is present in aquatic environment at concentrations beyond permissible limit. Considering the fact that toxic effects are function of the exposure concentration, studies involving toxicological risk assessment should be done at environmentally relevant concentration. Therefore we studied the toxic effects of Cr [VI] to zebrafish at an environmentally relevant concentration (2 mg L). We monitored the genotoxic potential of Cr [VI] in erythrocytes through a simple reliable microscopic assay and found an increase in frequency of micronucleated erythrocytes along with erythrocytes with blebbed, lobed and notched nuclei. In addition, Cr [VI] induced neurotoxicity, being a least reported event was also investigated. Histological alterations in brain, elevated GSH and MDA content and increased catalase activity indicated oxidative stress-mediated damage. This was further confirmed through expressional alteration of Ucp2. Upregulation of Nrf2, Nqo1 and Ho1 clearly indicated the involvement of Nrf2-ARE system in stress response against Cr [VI] induced neurotoxicity. The transcriptional induction of apoptotic genes such as Bax, Caspase 9 and Caspase 3 along with downregulation of Bcl2 indicated that the cytoprotective system failed to counter the induced stress. Interestingly, there was upregulation of AChE gene, which could be correlated with the upregulated apoptotic genes. This study provides an insight on the neurotoxic stress of Cr [VI] on the zebrafish yet at an environmentally relevant concentration. Moreover the induction of nuclear anomalies in the erythrocytes can serve as extremely sensitive endpoints of toxicological stress indicators of aquatic contaminants like Cr [VI].