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Polystyrene microplastics impact on cardiac and pulmonary physiology and microenvironment in a mouse model: Role of taurine supplementation and molecular docking insights
Summary
Researchers investigated the effects of polystyrene microplastics on heart and lung tissues in mice and found that exposure disrupted antioxidant defenses, increased lipid peroxidation, and elevated cardiac injury markers and pro-inflammatory cytokines. Microplastic exposure also upregulated inflammatory and pyroptotic gene expression in both tissues. Co-administration of taurine significantly ameliorated these alterations, suggesting it may offer protective effects against microplastic-induced cardiopulmonary damage.
Polystyrene microplastics (PS-MPs) have recently gained attention as widespread environmental contaminants posing risks to both human and animal health. In this study, we investigated the potential protective effect of taurine (200 mg/kg b.wt) against cardiopulmonary toxicity induced by PS-MPs (10 mg/kg b.wt) in male Swiss mice following a 60-day oral exposure. Molecular docking investigation for both proteins and mRNA targets was carried out utilizing a global, flexible docking strategy that allowed for full ligand conformational freedom and binding surface exploration. We designed an experimental model comprising four groups: Control, Taurine, PS-MPs, and a combined group (PS-MPs + Taurine). The results indicated that taurine significantly protected against PS-MPs-induced biochemical, histopathological, and molecular alterations that occurred in the cardiac and pulmonary tissues of mice. PS-MPs exposure disrupted the redox balance by suppressing enzymatic antioxidants (CAT, SOD, GPx) and increasing lipid peroxidation, while elevating cardiac injury markers (LDH, CK-MB, CPK, cTnI). These oxidative changes were accompanied by increased pro-inflammatory cytokines (TNF-α, IL-1β) in both tissues, histopathological lesions in the heart and lungs, and upregulation of gene expressions of inflammatory and pyroptotic mediators (NLRP3, Caspase-1, ASC, GSDMD, NF-κB, COX-2, IL-1β, IL-18). Co-administration of taurine with PS-MPs markedly ameliorated these alterations, restoring antioxidant defenses, reducing lipid peroxidation and cytokine levels, downregulating inflammasome and pyroptosis-related gene expression, and improving tissue architecture. Molecular docking supported these findings by showing taurine's potential interactions with inflammatory mediators, while styrene exhibited affinity for antioxidant enzymes, consistent with in vivo oxidative disruption. Collectively, the study highlights oxidative stress and inflammation as key mechanisms of PS-MPs-induced cardiopulmonary toxicity and highlights taurine's promise as a protective agent against microplastics-related health risks.
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