Photoaging of Facial Scrub Microbeads Causes Neurobehavioral Impairment in Zebrafish Larvae through Mitochondrial Dysfunction and Neurotransmission Disruption

Personal-care-product-derived microbeads are an important source of primary microplastics (MPs), yet their environmental transformation and toxicity remain unclear. Here, facial scrub (FS) microbeads were subjected to simulated photoaging and evaluated in zebrafish larvae at an environmentally relevant concentration. Photoaging promoted the formation of environmentally persistent free radicals (EPFRs), altered FS physicochemical properties, and enhanced the release of organic additives and heavy metals. Compared to virgin FS, photoaged FS (FS-60) induced stronger neurobehavioral impairment, including reduced tail coiling, swimming activity, and inner zone duration, mainly driven by leachates and EPFR-associated reactivity. Transcriptomic and biological analyses revealed disrupted mitochondrial function and neuronal signaling. FS-60 impaired central nervous system and motor neuron development, altered neurotransmitter levels (acetylcholine, serotonin, and γ-aminobutyric acid), and downregulated neurodevelopment-related genes. Moreover, FS-60 induced mitochondrial dysfunction, as supported by TEM-observed mitochondrial structural damage, elevated reactive oxygen species (ROS) and cytochrome c release, reduced ATP production and NAD + /NADH ratios, and suppressed electron-transport-chain-related genes. Mitoquinone mesylate (MitoQ) significantly alleviated locomotor deficits and ROS accumulation, confirming mitochondrial dysfunction as a key driver of FS-induced neurotoxicity. This study demonstrates that photoaging amplifies the neurotoxicity of cosmetic microbeads and should be considered in ecological risk assessment.