Brain targeted luteolin-graphene oxide nanoparticle abrogates polyethylene terephthalate induced altered neurological response in zebrafish

• Published in: Molecular biology reports 2024-12, Vol.51 (1), p.27-27, Article 27
• Main Authors: Guru, Ajay, Murugan, Raghul, Almutairi, Bader O., Arokiyaraj, Selvaraj, Arockiaraj, Jesu
• Format: Article
• Language: English
• Subjects: Acetylcholinesterase; Animal Anatomy; Animal Biochemistry; Biomedical and Life Sciences; Cell death; Cognitive ability; Danio rerio; Gene expression; Graphene; Health risk assessment; Health risks; Histology; Inflammation; Life Sciences; Lipid peroxidation; Morphology; Nanoparticles; Natural products; Neuroprotection; Neurotoxicity; Nitric oxide; Original Article; Oxidative stress; Polyethylene terephthalate
• ISSN: 0301-4851; 1573-4978
• DOI: 10.1007/s11033-023-08960-x

Background Polyethylene terephthalate (PET), a commonly used polymer in various food and plastic bag containers, has raised significant concerns regarding its environmental and human health risks. Despite its prevalent use, the impact of PET exposure on aquatic environments and its potential to induce neurotoxic conditions in species remain poorly understood. Furthermore, the mechanisms underlying amelioration through natural product intervention are not well-explored. In light of these gaps, our study aimed to elucidate the neurotoxic effects of PET in zebrafish through waterborne exposure, and to mitigate its neurological impact using luteolin-graphene oxide nanoparticles. Methods and Results Our investigation revealed that exposure to PET in water triggered adverse effects in zebrafish larvae, particularly in the head region. We observed heightened oxidative stress, lipid peroxidation, and cell death, accompanied by impaired antioxidant defense enzymes. Furthermore, abnormal levels of acetylcholine esterase and nitric oxide in the zebrafish brain indicated cognitive impairment. To address these issues, we explored the potential neuroprotective effects of luteolin-graphene oxide nanoparticles. These nanoparticles demonstrated efficacy in localizing within the zebrafish brain, enhancing their therapeutic impact against PET exposure. Treatment with luteolin-graphene oxide nanoparticles not only mitigated PET-induced neurological alterations but also exhibited a neuroprotective effect. This was evidenced by the regulation of pro-inflammatory cytokine gene expression in the zebrafish brain. Additionally, normalization of locomotory behavior in PET-exposed zebrafish following nanoparticle treatment underscored the potential effectiveness of luteolin-graphene oxide nanoparticles as a treatment against PET-induced neurotoxicity. Conclusions In summary, our study emphasizes the urgent need to investigate the environmental and health risks associated with PET. We demonstrate the potential of luteolin-graphene oxide nanoparticles as an effective intervention against PET-induced neurotoxicity in zebrafish.