The Metal–Organic Framework NH ₂ -MIL-101(Fe) Modulates Arsenate Bioaccumulation, Biotransformation, Trophic Transfer, and Mitochondrial Genotoxicity in <i>Daphnia magna</i> -Zebrafish Food Chain

Metal-organic frameworks (MOFs) are promising adsorbents for arsenate (As(V)) remediation; however, their ecological risks during co-occurrence with As(V) in aquatic ecosystems remain poorly understood. This study investigated the effects of NH₂-MIL-101(Fe) on As(V) bioaccumulation, trophic transfer, biotransformation, and mitochondrial genotoxicity across generations using a <i>Daphnia magna</i>-<i>Danio rerio</i> (zebrafish) food chain exposure model consisting of a 14 day exposure and a 26 day depuration phase. NH₂-MIL-101(Fe) increased total arsenic bioaccumulation in <i>D. magna</i> (15.2-fold) and zebrafish tissues (2.0-18.6-fold at day 14 and 2.6-33.8-fold at day 40), while reducing the biomagnification factor from 0.045 to 0.026. It promoted arsenic uptake, likely via oxidative-stress-mediated upregulation of <i>aqp</i>7 and formation of As(V)-MOF complexes, and enhanced As(V) secondary methylation, associated with <i>as</i>3<i>mt</i> upregulation. Co-exposure increased zebrafish mitochondrial DNA (mtDNA) damage through inducing excessive reactive oxygen species and inhibiting antioxidant enzymes, accompanied by adenosine triphosphate depletion and locomotor decline. The mtDNA damage was transmitted to offspring, demonstrating multigenerational mitochondrial toxicity. These findings reveal that NH₂-MIL-101(Fe)-As(V) coexposure increased arsenic burden across trophic levels, particularly in lower trophic levels, and amplifies heritable mitochondrial genotoxicity in aquatic food chains.