Benzotriazole ultraviolet stabilizers (BUVSs) are widespread emerging pollutants, which can pose exposure risks to benthic organisms. However, the toxicity and mechanisms of BUVSs congeners in benthic clams are far from elucidated. In this study, Asian clams (Corbicula fluminea) were exposed to one of UV-234, UV-326, UV-329, or UV-P at environmentally relevant levels (0.1, 1, and 10 μg/L) for 21 days. Filtration rate (FR) was increased in clams exposed to all BUVSs and there were notable histopathologic changes, including irregular digestive lumen, lipid droplet vacuolation, and degraded epithelial cells. To determine the molecular underpinnings following BUVSs exposure, the transcriptome responses in digestive glands were compared. Differentially expressed genes shared among BUVSs treatments were associated with focal adhesion, TNF-α/NF-κB proinflammatory pathways, and apoptosis. Following this, biochemical analysis of biomarkers related to apoptosis were conducted to further validate response. Exposure to BUVSs inhibited anti-oxidant enzyme activity and induced oxidative stress. Heat shock proteins were also triggered with exposure, and there was an induction of caspase-3 and caspase-9 activity. Molecular responses were not identical in the digestive gland of C. fluminea when comparing responses to BUVSs; nevertheless conserved mechanism (impairment of the oxidative defense system, immune system disruption, and induction of apoptosis) among BUVSs congeners was noted. This study provides novel insight into the toxicity and hazards of BUVSs in benthic organisms.
Keywords: Benzotriazole ultraviolet stabilizers; Corbicula fluminea; Focal adhesion; Siphoning behavior; TNF mediated apoptosis.
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