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The effects of microplastics exposure on quail's hypothalamus: Neurotransmission disturbance, cytokine imbalance and ROS/TGF-β/Akt/FoxO3a signaling disruption
Summary
Japanese quail exposed to polystyrene microplastics for five weeks showed significant brain damage in the hypothalamus, including structural changes to neurons, disrupted chemical signaling, and inflammation. The microplastics caused oxidative stress and interfered with important cell-survival pathways in the brain. While studied in birds, these neurotoxic effects are relevant because similar brain pathways exist in humans, and they suggest microplastic exposure could affect neurological function.
Microplastics (MPs) have become a major focus of environmental toxicology, raising concerns about their potential adverse effects on animal organs and body systems. As these tiny particles infiltrate ecosystems, they may pose risks to the health of organisms across diverse species. In this study, we attempted to examine the neurotoxic effects of MPs exposure on avian hypothalamus by using an animal model-Japanese quail (Coturnix japonica). The quails of 7-day-old were exposed to 0.02 mg/kg, 0.4 mg/kg and 8 mg/kg polystyrene microplastic (PS-MPs) of environmental relevance for 35 days. The results showed PS-MPs exposure did damages to hypothalamic structure characterized by neuron malformation, irregular arrangement and cellular vacuolation after 5-week exposure. PS-MPs exposure also induced Nissl body reduction and dissolution in the hypothalamus. Moreover, the decrease of acetylcholinesterase (AchE) activity and increasing acetylcholine (Ach) indicated that PS-MPs exposure caused hypothalamic neurotransmission disturbance. PS-MPs exposure also led to neuroinflammation by disrupting the balance between proinflammatory and anti-inflammatory cytokines. Moreover, increasing reactive oxygen species (ROS) and malondialdehyde (MDA) generation with reducing antioxidants indicated PS-MPs led to hypothalamic oxidative stress. Additionally, RNA-Seq analysis found that both transforming growth factor-β (TGF-β) signaling and forkhead box O (FoxO) signaling were disturbed in the hypothalamus by PS-MPs exposure. Especially, the increasing ROS led to TGF-β activation and then induced hypothalamic inflammation by nuclear factor κB (NF-κB) activation. The present study concluded that oxidative stress might be an important mechanistic signaling involved in MPs neurotoxicology.
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