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Abamectin causes cardiac dysfunction in carp via inhibiting redox equilibrium and resulting in immune inflammatory
Panpan Zhao1, Yan Wang2, Qiankun Yang1,3
1Institute of Neuroscience, The First People's Hospital of Lianyungang, Lianyungang, 222000, China.
Abstract:
This study aims to investigate the effects of environmentally relevant concentrations of abamectin on the cardiac function of carp and the potential mechanisms. Here, male carp were exposed to abamectin, and cardiac function-related enzymatic markers were examined. Cardiac histopathology, redox equilibrium, inflammation, and cell death were evaluated. Abamectin exposure caused cardiac dysfunction by upregulating lactate dehydrogenase (LDH), aspartate aminotransferase (AST), creatine kinase (CK), creatine Kinase MB isoenzyme (CK-MB) and white blood cells (WBCs), and decreasing red blood cells (RBCs) and hemoglobin (Hb). DHE staining and biochemical assays revealed that abamectin caused ROS release and oxidative stress by inhibiting Nrf2-ARE pathway. Histopathological and real-time fluorescence quantitative PCR (RT-qPCR) assays revealed that abamectin caused myocardial fiber swelling and inflammatory cell infiltration, enhanced pro-inflammatory cytokines tumor necrosis factor-α (Tnf-α), interleukin-1 beta (Il-1β), and Il-6 levels and attenuated anti-inflammatory cytokines Il-10 and transforming growth factor beta 1 (Tgf-β1) through activating NOD-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome and nuclear factor kappa-B (NF-κB) pathway. Tunel staining showed that abamectin triggered cardiac apoptosis via activating p53-mediated mitochondrial apoptosis with elevated bcl2-associated X (Bax), reduced B-cell lymphoma-2 (Bcl-2), and activated Caspase-9 and Caspase-3. Immunoblot analysis revealed that abamectin activated autophagic flow by inhibiting mammalian target of rapamycin (mTOR), resulting in the conversion of LC3B from LC3-I to LC3-II, elevation of autophagy protein 5 (Atg5), and reduction of p62. Overall, abamectin caused cardiac dysfunction in carp via inhibiting redox equilibrium and resulting in immune inflammatory response and programmed cell death.
Insights
Abamectin exposure harms carp heart function by disrupting oxidative balance, triggering inflammation, and causing cell death through various molecular pathways. This pesticide poses a significant risk to aquatic life, impacting cardiac health.
Area of Science:
- Environmental Toxicology
- Cardiovascular Physiology
- Molecular Mechanisms of Toxicity
Background:
- Pesticides like abamectin are increasingly detected in aquatic environments.
- Understanding the sub-lethal effects of abamectin on non-target aquatic organisms is crucial for ecological risk assessment.
- Carp (Cyprinus carpio) are a common freshwater fish species susceptible to environmental contaminants.
Purpose of the Study:
- To investigate the cardiac effects of environmentally relevant abamectin concentrations in carp.
- To elucidate the underlying molecular mechanisms of abamectin-induced cardiotoxicity.
- To assess the impact on oxidative stress, inflammation, and cell death pathways.
Main Methods:
- Carp were exposed to abamectin.
- Cardiac function markers (enzymes, blood cells) were analyzed.
- Histopathology, oxidative stress (DHE, Nrf2-ARE), inflammation (NLRP3, NF-κB), apoptosis (p53, Bax, Bcl-2, Caspases), and autophagy (mTOR, LC3B) were evaluated.
Main Results:
- Abamectin exposure led to cardiac dysfunction, indicated by altered enzymatic markers and blood cell counts.
- It induced oxidative stress by inhibiting the Nrf2-ARE pathway.
- Abamectin triggered myocardial inflammation via NLRP3 inflammasome and NF-κB activation, and induced apoptosis through the p53-mediated mitochondrial pathway.
- Autophagic flow was activated by inhibiting mTOR.
Conclusions:
- Abamectin causes significant cardiac dysfunction in carp.
- The toxicity involves inhibition of redox equilibrium, induction of inflammatory responses, and promotion of programmed cell death.
- These findings highlight the cardiotoxic potential of abamectin in freshwater fish.
