We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
ROS-driven crosstalk between ferroptosis and necroptosis mediates neurotoxicity induced by maternal exposure to polystyrene nanoplastics in zebrafish
AI summary Read the abstract
Adult female zebrafish were exposed to polystyrene nanoplastics for 28 days. The particles passed to their embryos and larvae, which had lower hatching rates, more malformations, reduced movement and fewer neurons in part of the brain. The damage was driven by oxidative stress and two cell-death pathways, and antioxidant treatment partly reversed it.
The pervasive environmental distribution of nanoplastics (NPs) raises critical concerns regarding their offspring health impacts. However, the precise mechanisms underlying neurotoxicity induced by maternal exposure to NPs remain poorly understood. In this study, adult female zebrafish were exposed to polystyrene nanoplastics (PS-NPs; 0.1 and 1 mg/L) for 28 days to investigate maternal transfer, subsequent neurotoxic effects, and associated cell death pathways in offspring. Fluorescence imaging confirmed the concentration-dependent accumulation of maternally transferred PS-NPs in embryos and larvae. Consequently, maternal exposure to PS-NPs significantly reduced fertilization and hatching rates, increased malformation incidence, and impaired larval development. Behavioral analyses revealed decreased locomotor activity and impaired light-dark responsiveness, accompanied by structural neuronal disorganization and reduced neuronal density in the telencephalon. Transcriptomic and molecular analyses indicated that maternal exposure to PS-NPs severely disrupted iron homeostasis characterized by iron overload and excessive reactive oxygen species (ROS) burst, and lipid peroxidation, which concurrently altered the expression of critical genes related to ferroptosis and necroptosis. Antioxidant intervention using N-acetylcysteine (NAC) effectively alleviated oxidative stress and rescued alterations in ferroptosis and necroptosis, while ferrostatin-1 (Fer-1) improved iron homeostasis, attenuated neuronal injury, and mitigated necroptosis-related responses. Collectively, our findings suggest that ROS-associated ferroptosis and necroptosis contribute to offspring neurotoxicity induced by maternal exposure to PS-NPs and indicate a potential functional crosstalk between these two regulated cell death pathways. This study provides new insights into the mechanisms underlying offspring neurotoxicity induced by NPs.
More Papers Like This
Impact of polystyrene nanoplastics on apoptosis and inflammation in zebrafish larvae: Insights from reactive oxygen species perspective
AI summary Read the abstract
Researchers showed that polystyrene nanoplastics accumulate in zebrafish larvae and trigger excessive reactive oxygen species production via NADPH oxidase upregulation, causing mitochondrial dysfunction, apoptosis, and NF-κB-driven inflammation — with inhibiting ROS generation effectively blocking downstream cell death and inflammatory responses.
Polystyrene microplastics and nanoplastics induce neurotoxicity in zebrafish via oxidative stress and neurotransmitter disruption
AI summary Read the abstract
Researchers exposed zebrafish embryos to polystyrene micro- and nanoplastics and found that both particle sizes caused neurodevelopmental toxicity, with nanoplastics being more potent. The plastic particles induced oxidative stress in the brain and disrupted neurotransmitter levels critical for normal neural development. The study suggests that microplastic and nanoplastic contamination in aquatic environments may pose significant risks to the neurological development of fish.
Maternal exposure to nanopolystyrene induces neurotoxicity in offspring through P53-mediated ferritinophagy and ferroptosis in the rat hippocampus
AI summary Read the abstract
When pregnant and nursing rats were fed nanoplastics, their offspring showed impaired learning and memory due to a specific type of cell death called ferroptosis in the brain's hippocampus. The nanoplastics triggered a chain reaction involving oxidative stress and iron buildup that damaged developing brain cells, suggesting that maternal exposure to nanoplastics during pregnancy and breastfeeding could harm offspring brain development.
Polystyrene Nanoplastic Exposure Induces Developmental Toxicity by Activating the Oxidative Stress Response and Base Excision Repair Pathway in Zebrafish (Danio rerio)
AI summary Read the abstract
Researchers exposed zebrafish embryos to polystyrene nanoplastics at various concentrations and found significant developmental abnormalities including reduced hatching rates and increased malformations. The nanoplastics activated oxidative stress responses and DNA repair pathways, indicating cellular damage during critical early development stages. The study provides mechanistic evidence for how nanoplastic exposure can disrupt normal embryonic development in aquatic organisms.
Effects of polystyrene nanoplastic size on zebrafish embryo development
AI summary Read the abstract
Researchers exposed zebrafish embryos to polystyrene nanoplastics of four sizes and found only the smallest (30 nm) caused mortality and altered oxidative stress and apoptosis gene expression, while larger particles (100–450 nm) were ingested and accumulated in the digestive system without causing developmental malformations.
Research digests by email
When a large batch of papers lands in the Atlas, we read through it and send a short write-up of what stood out.