Micro- and nanoplastics disrupt the gut-liver-brain axis: mechanisms of multi-organ toxicity in animal models.

Micro- and nanoplastics (MNPs) are ubiquitous environmental contaminants increasingly recognized as potential drivers of systemic toxicity. Growing evidence indicates that MNPs may affect interconnected physiological systems, particularly the gut-liver-brain axis, which integrates metabolic, immunological, and neuroendocrine responses. This review summarizes current knowledge on the effects of MNPs on the gut-liver-brain axis based on animal studies, with emphasis on mechanisms of toxicity and inter-organ communication. Available findings indicate that the gastrointestinal tract is the primary site of interaction, where MNPs induce intestinal barrier disruption, oxidative stress, immune activation, and gut microbiota dysbiosis. These alterations may promote endotoxemia and inflammatory signaling, contributing to hepatic metabolic disturbances, mitochondrial dysfunction, and hepatocellular injury. In parallel, MNPs may affect the central nervous system through neuroimmune responses, altered neurotransmission, blood-brain barrier dysfunction, and gut-brain signaling disturbances. Oxidative stress, chronic inflammation, and disrupted inter-organ communication appear to represent central mechanisms underlying MNPs toxicity. Nanoplastics, due to their higher bioavailability and ability to cross biological barriers, exhibit particularly strong toxic potential. Overall, current evidence supports a systems-level view of MNPs toxicity and highlights the importance of integrative approaches for improving environmental and health risk assessment.