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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
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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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Researchers found that polystyrene microplastics caused liver damage in an animal model through oxidative stress and lipid metabolic disruption, and that taurine supplementation exerted a protective effect by modulating oxidative and metabolic pathways. The results support taurine as a potential therapeutic agent for microplastic-induced hepatotoxicity.
Table 1_Palliative effect of taurine against hepatic injury induced by polystyrene microplastics through antioxidant and metabolic pathway modulation in mice.docx
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This study investigated the molecular mechanisms underlying liver toxicity caused by polystyrene microplastics, finding that PS-MPs accumulated in hepatic tissues and disrupted lipid metabolism through oxidative stress and inflammatory signaling. The results mapped specific molecular pathways through which microplastics impair liver function.
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Researchers exposed mice to oral polystyrene microplastics for 60 days and documented kidney damage through oxidative stress, inflammation, apoptosis, and fibrosis, then showed that taurine supplementation could substantially reverse these effects by restoring antioxidant defenses and suppressing pro-inflammatory signaling pathways.
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Mice exposed to microplastics showed damage to their spleen (a key immune organ), including increased inflammation, cell stress, and cell death—but the amino acid taurine, a common supplement ingredient, helped protect against much of this damage. While this is animal research and more studies are needed before we know if it applies to humans, it hints that a cheap, widely available nutrient might one day help offset some health risks from the microplastics we're increasingly exposed to in daily life.
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Male Wistar rats orally dosed with polyethylene microplastics for 28 days showed elevated cardiac and pulmonary injury biomarkers, suppressed antioxidant defenses, inhibited mitochondrial TCA cycle enzymes, and disrupted respiratory chain complexes, indicating simultaneous heart and lung damage through shared oxidative and inflammatory pathways. The study suggests that routine microplastic ingestion may impose systemic cardiopulmonary stress, with organ-specific dose-response differences suggesting the lungs may be particularly sensitive.
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