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Protective effects of taurine against microplastic-induced nephrotoxicity through suppression of oxidative stress, NF-κB/Caspase-3 activation, and pro-fibrotic signaling
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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.
Microplastic (MPs) pollution has emerged as a major global concern due to its potential impacts on human and animal health. In this 60-day oral study, male Swiss mice were exposed to polystyrene microplastics (Ps-MPs; 10 mg/kg b.wt), and the protective efficacy of taurine (Tau; 200 mg/kg b.wt) was assessed with particular focus on renal function, oxidative stress, inflammation, apoptosis, fibrosis, and gene expression. Ps-MPs exposure markedly disrupted kidney function, as indicated by reduced total protein alongside elevated serum creatinine, urea, and uric acid. Renal homogenate analysis revealed enhanced lipid peroxidation, evidenced by increased malondialdehyde, accompanied by suppressed antioxidant defenses (catalase, superoxide dismutase, and glutathione peroxidase). Gene expression profiling demonstrated significant upregulation of pro-inflammatory, apoptotic, and fibrotic mediators (tumor necrosis factor-alpha, interleukin-1β, alpha-smooth muscle actin, transforming growth factor-beta 1, and sterol regulatory element-binding protein-1), alongside downregulation of metabolic and antioxidant regulators (peroxisome proliferator-activated receptor alpha, AMP-activated protein kinase, and sirtuin 1). Immunohistochemical analysis further revealed increased Caspase-3 and nuclear factor kappa B immunoexpression in renal tissue, indicating enhanced apoptosis and inflammation. Histochemical staining showed pronounced collagen deposition using Masson's trichrome stain, accompanied by architectural disruption as evidenced by periodic acid-Schiff staining, confirming Ps-MPs-induced renal fibrosis and structural damage. Taurine supplementation effectively counteracted these Ps-MPs-induced alterations by restoring serum biochemical parameters, re-establishing antioxidant balance, suppressing inflammatory, apoptotic, and fibrotic signaling, and normalizing collagen distribution and renal histoarchitecture. These results propose that Tau supplementation may serve as a promising therapeutic agent to mitigate Ps-MPs-induced nephrotoxicity.
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