Benzotriazole UV stabilizer-induced genotoxicity in freshwater benthic clams: A survey on apoptosis, oxidative stress, histopathology and transcriptomics

Benzotriazole UV stabilizer-329 (UV-329) is frequently detected in various environmental and biological matrices. However, the toxicity effect on freshwater benthos induced by UV-329 has rarely been described. In this study, genotoxicity, apoptosis, oxidative stress, histopathological alterations, siphoning behavior, and bioaccumulation in the gill and digestive gland of Corbicula fluminea exposed to UV-329 at 10, 100, and 1000 μg/L for 21 days were investigated. Toxicity screening using transcriptomics confirmed that UV-329 preferentially stimulated cellular process-related pathways including gap junctions, apoptosis, phagosomes and necroptosis. The transcript levels of a large number of apoptosis genes were significantly upregulated. This apoptosis mechanism was further confirmed by the fact that UV-329 exposure significantly increased the percentage of apoptotic cells, activated caspase-3, -8, and -9, and affected the antioxidant enzyme activities. Following exposure to 1000 μg/L UV-329, significant histological alterations were reflected in the corrosion of cilia, cellular swelling of epithelial cells in the gills, degeneration of digestive tubules, and necrosis of epithelial cells in the digestive glands. These results may aid in elucidating the toxicity mechanism of UV329 in bivalves and evaluating the hazards of UV-329 in benthic ecosystems.