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In silico insights into microplastic additive toxicity: Risks of pulmonary fibrosis and endocrine disruption
Summary
Researchers used computational modeling to investigate how five common microplastic additives, including phthalates and flame retardants, interact with proteins involved in lung fibrosis and endocrine function. Molecular docking revealed that these additives bind strongly to fibrotic markers like TGF-beta and to hormone receptors, suggesting potential mechanisms for tissue damage and hormonal disruption. The study highlights the need for further investigation into the health risks posed by chemical additives leaching from microplastics.
Microplastics and their constituent chemicals, such as phthalates, bisphenols, and flame retardants, have emerged as a significant toxin negatively affecting fibrotic potential and functioning of the endocrine system in human beings. With an objective to find out the principal molecular mechanisms and nature of interaction with key endocrine and fibrotic proteins, the impacts of five frequently used microplastic additives were studied. The molecular docking, protein-protein interaction networks, and gene interaction tools were employed to study the impacts. Pharmacokinetics, toxicity prediction, and ADME profiling and systemic risks were analysed using ProTox-II and Swiss ADME. The docking results revealed significant binding tendencies of microplastics components with fibrotic markers (TGF-β1, Smad3) and nuclear hormone receptors (ERα, AR). Network analysis indicated overlapping molecular pathways of extracellular matrix remodelling, and TGF-β/Smad signaling as key points of interaction. The present investigation indicated the strong connection between endocrine disruption and pulmonary fibrosis, mediated through shared signalling pathways. The present investigation revealed that microplastics and their additives exert adverse human health risks, demanding stringent environmental legislation and environmentally benign chemicals as a substitute for microplastic additives. In silico methods revealed significant insights into the molecular basis of ecotoxicity, emphasising the immediate requirement for further research to help interpret the chronic effects of microplastic pollution.
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