Hepatotoxicity of benzotriazole and its effect on the cadmium induced toxicity in zebrafish Danio rerio

- 5.0μM of 1H-BTR induced no acute physiology toxic effects on zebrafish embryo.
- 1H-BTR induced increasing expression of liver-specific fatty acid binding protein.
- Co-exposure to 1H-BTR could decrease the toxicity of Cd in zebrafish.
- Cd bioaccumulation increased significantly in zebrafish pre-exposed to 1H-BTR.

As an emerging contaminant, 1-H-benzotriazole (1H-BTR) has been detected in the engineered and natural aquatic environments, which usually coexists with heavy metals and causes combined pollution. In the present study, wild-type and transgenic zebrafish Danio rerio were used to explore the acute toxicity as well as the single and joint hepatotoxicity of cadmium (Cd) and 1H-BTR. Although the acute toxicity of 1H-BTR to zebrafish was low, increased expression of liver-specific fatty acid binding protein was observed in transgenic zebrafish when the embryos were exposed to 5.0 μM of 1H-BTR for 30 days. Besides, co-exposure to 1H-BTR not only reduced the acute toxic effects induced by Cd, but also alleviated the Cd-induced liver atrophy in transgenic fish. Correspondingly, effects of combined exposure to 1H-BTR on the Cd-induced expressions of several signal pathway-related genes and superoxide dismutase and glutathione-s-transferase proteins were studied. Based on the determination of Cd bioaccumulation in fish and the complexing stability constant (β) of Cd-BTR complex in solution, the detoxification mechanism of co-existing 1H-BTR on Cd to the zebrafish was discussed.

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