Exploring the Combined Effect of Exercise and Apigenin on Aluminium-Induced Neurotoxicity in Zebrafish.

Aluminium (AL) is a strong environmental neurotoxin linked to neurodegenerative disorders. Widespread industrial use leads to its presence in water systems, causing bioaccumulation in organisms. This, in turn, results in the bioaccumulation of AL in various organisms. Several studies have highlighted the benefits of enhanced physical activity in combating neurodegenerative diseases. Meanwhile widespread presence of apigenin in aquatic environment has been largely overlooked, in terms of its potential to counter AL-induced neurotoxicity. The combined impact of exercise and apigenin in mitigating the effects of AL-induced neurotoxicity in aquatic animals remains unexplored. Hence, the objective of this study is to determine whether the combined treatment of exercise and apigenin can effectively alleviate the chronic neurotoxicity induced by AL. Zebrafish that were exposed to AL showed behaviours resembling anxiety, increased aggression, unusual swimming pattern, and memory impairment, which are typical features observed in Alzheimer's disease (AD)-like syndrome. Combined treatment of exercise and apigenin protects zebrafish from AL-induced neurotoxicity, which was measured by improvements in memory, reduced anxiety and aggression, and increased levels of antioxidant enzymes and acetylcholinesterase (AChE) activity. Furthermore, AL exposure is associated with increased expression of genes related to neuroinflammation and AD. However, synergistic effect of exercise and apigenin counteract this effect in AL-treated zebrafish. These findings suggest that AL is involved in neurodegenerative diseases in fish, which could affect the integrity of aquatic ecosystem. Hence, there is a strong correlation between enhanced physical activity, apigenin, and the well-being of the ecosystem.

Combined effects of a high-fat diet and polyethylene microplastic exposure induce impaired lipid metabolism and locomotor behavior in larvae and adult zebrafish.

Microplastics (MP), tiny plastic particles, can be ingested by fish through their habitat or contaminated food sources. When combined with a high-fat diet (HFD), MP exposure may lead to increased MP accumulation in fish and negative impacts on their health. However, the underlying mechanisms of how MP and HFD interact to promote fat accumulation in fish remain poorly understood. In this study, we aimed to evaluate the combined effect of HFD and polyethylene MP (PE-MP) in the zebrafish model (Danio rerio) and decipher its molecular mechanisms. Adult zebrafish exposed to the combined HFD and PE-MP showed elevated lipid accumulation, total cholesterol, triglycerides, and abnormal swimming behavior compared to HFD-fed fish. Histological and gene expression analysis revealed severe hepatic inflammation and injury, resembling nonalcoholic fatty liver disease (NAFLD) in the HFD + PE-MP exposed zebrafish. Moreover, HFD and PE-MP exposure upregulated genes related to lipogenesis (SREBP1, FAS, and C/EBPα) and inflammation (tnfα, il1ß, and il-6) in the liver. These findings underscore the interactive effect of environmental pollutants and fish diet, emphasizing the importance of improving fish culture practices to safeguard fish health and human consumers from microplastic contamination through the food chain. This research sheds light on the complex interactions between microplastics and diet, providing valuable insights into the potential risks of microplastic pollution in aquatic ecosystems and the implications for human health. Understanding the underlying molecular mechanisms will contribute to international research efforts to mitigate the adverse effects of microplastics on both environmental and public health.