Taurine mitigates oxidative stress, thyroid dysfunction and renal damage in silver nanoparticles-treated rats

Application of engineered silver nanoparticles (AgNPs) cuts across various fields including the biomedical industry and consumer product formulations, owing to their unique physicochemical characteristics. Similarly, AgNPs can originate from natural and human anthropogenic emissions, contributing to their environmental prevalence and persistence. However, research evidence has implicated AgNPs in renal toxicity. Taurine is a non-proteinogenic β-amino sulfonic acid, and has been demonstrated to elicit a plethora of cytoprotective activities. Hence, the potential protective effect of taurine on AgNPs-induced renal toxicity was investigated in this study. Adult male Wistar rats were allotted into five different experimental groups (n = 10) including control, taurine alone (100 mg/kg), AgNPs alone (200 µg/kg), AgNPs (200 µg/kg) + taurine (50 mg/kg), and AgNPs (200 µg/kg) + taurine (100 mg/kg). Taurine was administered orally while AgNPs was intraperitoneally administered to the animals for 21 days. AgNPs-exposed animals demonstrated significant elevation in serum levels of creatinine and urea, with a marked reduction in triiodothyronine (T3), thyroxine (T4) and T3/T4 ratio. In addition, the levels of oxidative stress indices increased significantly with a concomitant reduction of renal antioxidant enzymes following AgNPs treatment. Moreover, AgNPs administration induced inflammation and significant damage in renal tissues in the treated animals. Conversely, taurine co-treatment significantly reversed AgNPs-induced renal damage by increasing renal antioxidant enzyme activities, decreasing oxidative stress, inflammation, and serum creatinine and urea levels while improving the levels of T3 and T4. The biochemical, hormonal and histological data evidenced the renoprotective attributes of taurine, suggesting that it could be a therapeutic agent against AgNPs-induced renal toxicity.