Taurine attenuates polystyrene microplastic–associated oxidative stress, inflammation, and apoptotic changes in the spleen of mice

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Introduction: Microplastic (MP) contamination is an emerging environmental threat with potential adverse effects on oxidative stress, immune function, and inflammatory homeostasis. This study investigated the oxidative stress, pro-inflammatory, and immunotoxic effects of polystyrene microplastics (PMPs) and evaluated the protective role of the nutraceutical taurine (TN) in male Swiss mice following 60 days of oral exposure. Methods: Mice were assigned to four groups: control, PMPs (10 mg/kg b.wt.), TN-treated (200 mg/kg b.wt.), and PMPs + TN. Hematological parameters and serum immune markers, including immunoglobulins G and M (IgG and IgM), complement component 3 (C3), and nitric oxide (NO), were assessed. Splenic tissue was analyzed for oxidative stress markers, including malondialdehyde (MDA), catalase (CAT), and superoxide dismutase (SOD); pro-inflammatory mediators, including tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), and nuclear factor kappa B (NF-κB); apoptotic markers, including caspase-3 and B-cell lymphoma 2 (BCL-2); and immune-regulatory genes, including cluster of differentiation 4 and 8 (CD4 and CD8). Histopathology (hematoxylin and eosin (H&E) and periodic acid-Schiff (PAS) staining) and immunohistochemistry for cyclooxygenase-2 (COX-2) and caspase-3 were performed to evaluate structural alterations and inflammatory/apoptotic signaling in the spleen. Results: PMPs exposure induced significant hematological disturbances, systemic inflammation, immune alterations, and elevated NO levels. In splenic tissue, PMPs caused oxidative stress and inflammation, evidenced by increased MDA, and TNF-α levels and reduced CAT and SOD activities. Histological and immunohistochemical analyses revealed structural splenic damage with enhanced Caspase-3 and COX-2 expression, indicating elevated apoptosis and inflammatory signaling. Gene expression analysis revealed upregulation of IL-1β, TNF-α, NF-κB, and Caspase-3, and CD8, wheras BCL-2 and CD4 were significantly downregulated. Taurine supplementation effectively mitigated PMPs-induced effects by restoring hematological, alleviating immune alterations, enhancing antioxidant defenses, reducing inflammatory and apoptotic markers, and improving gene expression profiles. Conclusion: These findings demonstrated that TN exerts protective effects against PMPs-induced oxidative stress, inflammation, apoptosis, and immune-related alterations in splenic tissue. TN partially attenuated PMPs-induced immunotoxic and histopathological changes in this experimental mouse model, although further mechanistic, dose-response, and functional immune studies are required to confirm its potential therapeutic or nutraceutical applications against PMPs -induced toxicity.

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