Abstract
Triclosan (TCS) is used as an antimicrobial agent and has been widely dispersed and detected in the aquatic environment. However, it remains uncertain whether TCS is genotoxic or not. In this study, the acute toxicity of TCS in goldfish (Carassius auratus) was studied. Then, based on the results for acute toxicity, other goldfish were exposed to various concentrations of TCS (control, DMSO control, and 1/4, 1/2, and 1/8 LC50) for 14 days, and the effects on genetic toxicity were evaluated using micronucleus (MN) and nuclear abnormalities (NA) frequencies in peripheral blood and the comet assay in the liver of the goldfish. In addition, malondialdehyde (MDA), reduced glutathione (GSH), catalase (CAT), and total antioxidant capacity (T-AOC) in the liver were assayed to evaluate oxidative stress and the possible mechanism of genotoxicity. The 96 h median lethal concentration of TCS was 1111.9 µg/l. After 14 days of exposure, the MN and NA frequencies were significantly increased in peripheral blood of the TCS-treated groups compared with the solvent control, and the comet tail moment and MDA in the liver in the highest dose of TCS groups were also significantly high. Meanwhile, an evident change in GSH, CAT, and T-AOC of the liver was found as the TCS exposure concentration increased. The results showed that TCS caused oxidative stress and a genotoxic response in goldfish, suggesting that it presents a potential ecotoxicological risk to aquatic ecosystems.
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