Abstract
As a major neonicotinoid insecticide, thiacloprid (THCP) is frequently detected in aquatic environments worldwide due to its heavy use, posing potential threats to aquatic organisms. In this study, zebrafish (Danio rerio) embryos were exposed to THCP (1, 10, 100, 1000 and 10,000 μg/L) for 5 days and then recovered in THCP-free water for 20 days to investigate the effects of early-stage THCP exposure on the development, antioxidant defense, and neurotransmitter systems of zebrafish, and explore their recovery mechanism. The results show that THCP exposure induced developmental toxicity and oxidative stress in zebrafish. The hypoactivity, behavioral alterations (decreased avoidance and edge preference behaviors) and neurotoxicity were found throughout the exposure-recovery experiments. THCP exposure altered the expression of γ-aminobutyric acid (GABA)- and serotonin (5-HT)-related genes accompanied by the decrease in GABA and 5-HT contents. However, after recovery, GABA content returned to the control level, but 5-HT did not, indicating that only the serotonergic system was persistently disrupted. Overall, our results suggest that the disruption of the serotonergic system and oxidative stress may aggravate neurotoxicity and that the former was the main reason for the depressive-like behavior. This study could help to unravel the mechanisms of the behavioral alterations induced by early-stage THCP exposure in zebrafish.
Funder
the National Natural Science Foundation of China
the Key Watershed Environmental Protection Scientific Research Project of Anhui Province, China
Subject
Health, Toxicology and Mutagenesis,Public Health, Environmental and Occupational Health
Cited by
10 articles.
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