Tissue-specific responses to hexavalent chromium and acenaphthene co-exposure in zebrafish.

Hexavalent chromium [Cr(VI)] and acenaphthene (Ace) can co-occur in industrially affected aquatic environments, but their effects across target organs under co-exposure remain poorly characterized. Adult male zebrafish were exposed for 28 d to environmentally relevant or high sublethal concentrations of Cr(VI) and Ace, individually and in combination. Histopathological changes, oxidative-stress biomarkers, TUNEL staining, and the expression of inflammation- and apoptosis-related markers were assessed in brain and heart tissues. At the highest co-exposure concentrations, brain malondialdehyde increased by 113.22%, whereas glutathione levels and superoxide dismutase and catalase activities decreased by 27.89%, 21.25%, and 52.25%, respectively. High-dose Cr(VI) alone reduced cardiac glutathione levels and superoxide dismutase and catalase activities by 23.75%, 21.31%, and 14.00%, respectively. Several co-exposure groups showed greater oxidative, inflammatory, and apoptotic responses than the corresponding single-pollutant groups. At the highest co-exposure concentrations, cardiac IL-10 mRNA and protein abundance both decreased by more than 50%, whereas TUNEL-positive signals increased 11 to 14-fold in the brain and heart. Changes in Bax, Bcl-2, Caspase-3, Caspase-9, and p53 expression were consistent with the possible involvement of mitochondrial apoptosis. Overall, response magnitudes differed between tissues: the heart showed comparatively pronounced responses to high-dose Cr(VI), whereas the brain was more responsive to high-dose Ace for several endpoints. These findings support multi-organ assessment when evaluating the potential effects of Cr(VI) and Ace co-exposure in aquatic organisms.