Comparative Biochemistry and Physiology C-toxicology & Pharmacology最新文献

Amitriptyline (AMI), one of the widely used tricyclic antidepressants (TCAs), has become a pharmaceutical contaminant frequently detected in aquatic ecosystems. However, the impacts of AMI exposure and underlying mechanisms on fish are still limited. In this study, adult zebrafish (F0) were exposed to AMI at 0 (control), 0.8, and 8 μg/L for 14 days. Subsequently, the exposed zebrafish were paired for spawning, and their offspring (F1) were reared in an AMI-free medium until 5 days post-fertilization (dpf). This study aimed to assess variations in behaviors and neurotransmitter levels in both the F0 (at the end of the 14-day exposure) and F1 generations (at 5 dpf). As a result, waterborne AMI exposure significantly reduced the locomotor activity, frequency of body contact, and duration of chase in F0 zebrafish, and resulted in notable changes in monoamine neurotransmitter levels in their brains. Parental exposure to AMI significantly elevated the heart rate and eye movement but reduced the locomotor activity in the F1 zebrafish, also along with significant changes in monoamine neurotransmitters and acetylcholine. Furthermore, significant correlations between the changes in behavioral traits and neurotransmitter levels were identified in both F0 and F1 generations. Our findings confirm the critical role of monoamine modulation in the neurobehavioral toxicity of AMI on zebrafish and their offspring, and emphasize the importance of paying attention to its multigenerational effects on fish.

Non-invasive optical registration and subsequent analysis of heart rate (HR) and heart rate variability (HRV) in transparent aquatic animals have recently been proposed as convenient toxicological endpoints, well-suited for automation data acquisition and processing. This approach was evaluated in experiments involving juvenile Daphnia magna and zebrafish (Danio rerio) embryos exposed to glyphosate solutions (20 mg/L, 2 mg/L, 0.2 mg/L, and 0.02 mg/L) and imidacloprid solutions (30 mg/L, 3 mg/L, 0.3 mg/L, and 0.03 mg/L). The findings indicate that cardiac performance assessment is a promising approach for short-term toxicity evaluation. However, the sensitivity of this physiological endpoint to various external factors may limit its broader application. Results from the two model species highlight their differing sensitivities to the tested substances, emphasizing the need for thorough preliminary studies before establishing this method as a standardized toxicological tool. The potential development and improvement of techniques for assessing heart rate in zebrafish and daphnids are discussed.

Perillaldehyde (PAE), a prevalent flavoring agent, has raised safety concerns due to conflicting evidence regarding its toxicity. This study provides a comprehensive assessment of the developmental and neurotoxic effects of PAE in zebrafish, elucidating the underlying mechanisms of its toxicity. Results showed that PAE affected the viability and hatching rate of zebrafish at 96 h postfertilization with the 50 % lethal concentration (LC50) of 7.975 mg/L. Furthermore, exposed‌ to a non-lethal concentration of 4 mg/L PAE induced a spectrum of morphological abnormalities, such as pericardial edema, delayed yolk sac absorption, reduced body length, and microphthalmia. Behavioral observations revealed that PAE reduced motor ability, and was accompanied by an increase in spontaneous turning angle and angular velocity. Using the TG(elav13:EGFP) transgenic model, we observed the number of newborn neurons was reduced, indicating that PAE induced obvious neurotoxic effects. Additionally, this concentration facilitated the accumulation of reactive oxygen species (ROS) and malondialdehyde (MDA), concomitantly decreasing the activity of antioxidant enzymes. QRT-PCR analysis revealed that PAE down-regulated Nestin and Neurogenin1 gene expression, up-regulated Glipr1a and Nox1 gene expression, and inhibited the Nrf2/HO-1 pathway. Notably, co-administration of N-acetylcysteine (NAC), an inhibitor of oxidative stress, mitigated oxidative stress levels and partially ameliorated the neurotoxicity. These findings suggest that oxidative stress is the primary mediator of PAE-induced neurotoxicity. This study provides crucial insights for the safe application of PAE.