Epigallocatechin-gallate ameliorates polystyrene microplastics-induced oxido-inflammation and mitochondria-mediated apoptosis in testicular cells via modulation of Nrf2/HO-1, /mTOR/Atg-7, and Cx-43/NOX-1 levels

The study aimed to investigate the impact of Epigallocatechin-gallate (EGCG) on polystyrene microplastics (PS-MPs) induced reproductive anomalies in rats. To induce reproductive toxicity, PS-MPs were administered at a dose of 0.01 mg/kg/bw for several weeks. Following this, rats were treated with oral doses of 80 mg/kg/bw EGCG for 8 weeks. PS-MPs increase MDA levels while decreasing SOD, CAT, and GSH activity. EGCG administration reduces these effects. Inflammatory markers like NF-κB, IL-1β, TNF-α, NOX-1, and NLRP3 inflammasome are upregulated with PS-MPs but downregulated with EGCG treatment. Cx-43, Nrf2, HO-1, mTOR, and Atg-7 decrease with PS-MPs but increase with EGCG co-treatment. PS-MPs also increase NLRP3 levels, but EGCG treatment inhibits this effect. EGCG enhances sperm quality by raising motility, count, viability, and decreasing the ratio of aberrant and dead spermatozoa. Additional evidence for the reduced spermatogenesis was provided by histopathological scoring. Testicular tissue was subjected to PS-MP-induced oxidative stress, apoptosis, and inflammation; however, EGCG therapy reversed these effects and enhanced sperm quality. Overall, the PS-MPs-induced reproductive toxicity in rats appears to have potential for therapy with EGCG supplementation due to the modulation of Nrf2/HO-1, mTOR/Atg-7, and Cx-43/NOX-1 levels, as well as the prevention of mitochondria-mediated apoptosis and oxido-inflammation.