We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Early clues and molecular mechanism involved in neurodegenerative diseases induced in immature mice by combined exposure to polypropylene microplastics and DEHP
Summary
Researchers exposed young mice to polypropylene microplastics combined with DEHP, a chemical commonly found in plastics, and observed significant brain damage including memory problems and damage to the hippocampus. The combined exposure was worse than either substance alone, showing additive or synergistic toxic effects on the developing brain. This is particularly concerning for young children, who are most commonly exposed to polypropylene products and may be more vulnerable to these neurotoxic effects.
Studies have shown that exposure to either microplastics (MPs) or di-(2-ethylhexyl) phthalic acid (DEHP) alone can cause neurotoxicity in animals, but it remains uncertain whether and to what extent co-exposure to these two substances, which often occur together in reality, can also induce neurotoxicity. This study aimed to investigate the neurotoxicity and molecular mechanisms of combined exposure to DEHP and polypropylene microplastics (synthetic PP-MPs were used), the microplastics most commonly encountered by young children, in immature mice. The results showed that exposure to PP-MPs and/or DEHP did cause neurotoxic effects in immature mice, including induction of neurocognitive and memory deficits, damage to the CA3 region of the hippocampus, increased oxidative stress, and decreased AChE activity in the brain. The severity of the neurotoxicity increased with increasing concentrations of PP-MPs, combined exposure to PP-MPs and DEHP exhibited additive or synergistic effects. Transcriptomic analyses revealed that the PP-MPs and/or DEHP exposure altered the expression profiles of gene clusters involved in the stress response, and in protein processing in endoplasmic reticulum. Quantitative analyses further indicated that PP-MPs and/or DEHP exposure inhibited the activity of the heat shock response mediated by heat shock transcription factor 1, while chronically activated the unfolded protein response, consequently inducing neurotoxicity through neuronal apoptosis and neuroinflammation in the immature mice. As a pioneer study to highlight the neurotoxicity induced by combined exposure to PP-MPs and DEHP in immature mice, this research provides new insights into mitigating the health risks of PP-MPs and DEHP exposure in young children.
Sign in to start a discussion.
More Papers Like This
Adolescent exposure to micro/nanoplastics induces cognitive impairments in mice with neuronal morphological damage and multi-omic alterations
Adolescent mice exposed to polystyrene nanoplastics showed significant memory and learning problems, along with neuron loss and reduced new brain cell growth in the hippocampus. The nanoplastics also disrupted gut bacteria and brain chemistry, with strong links found between gut microbiome changes and brain metabolic disruption, suggesting that plastic exposure during youth may impair brain development through the gut-brain connection.
Early-life exposure to polypropylene nanoplastics induces neurodevelopmental toxicity in mice and human iPSC-derived cerebral organoids
Researchers exposed pregnant mice to polypropylene nanoplastics through inhalation and found that their offspring showed impaired brain development, poor spatial memory, reduced motor coordination, and increased anxiety. Tests using human brain organoids (lab-grown mini-brains) confirmed that nanoplastics disrupt the growth and differentiation of neurons, raising concerns about fetal brain health from plastic pollution during pregnancy.
Exposition to Plastic and Associated-chemicals in Neurodevelpmental Disorder: an Overview
This overview pools findings from multiple studies on how plastics and their associated chemicals may affect brain development in children. Exposure to micro- and nanoplastics, plasticizers like BPA, and flame retardants has been linked to neurodevelopmental conditions such as autism and ADHD in early research, though more human studies are needed to confirm these connections.
Di-(2-Ethylhexyl) Phthalate and Microplastics Induced Neuronal Apoptosis through the PI3K/AKT Pathway and Mitochondrial Dysfunction
Researchers found that the plasticizer DEHP and microplastics caused neuronal cell death in mice brains through the PI3K/AKT signaling pathway and mitochondrial dysfunction. The study demonstrated that combined exposure to DEHP and microplastics produced greater toxic effects on brain neurons than either substance alone, leading to changes in mitochondrial function and increased cell death.
Teratological, neurochemical and histomorphic changes in the limbic areas of F1 mice progeny due to co-parental polystyrene nanoplastic exposure
Researchers exposed parent mice to polystyrene nanoplastics before and during pregnancy and found that offspring exhibited skeletal and visceral malformations, impaired neonatal reflexes, learning deficits, and structural brain changes — including reduced hippocampal neurons — demonstrating transgenerational neurodevelopmental harm from nanoplastic exposure.