Kutlu, T.Kazak, F.Uyar, A.2024-09-182024-09-1820231792-2720https://doi.org/10.12681/jhvms.28802https://hdl.handle.net/20.500.12483/7572In the present study, it was aimed to examine the effects of early calcium oxalate (CaOx) crystal formation and deposition on the kidneys and the effects of alpha-lipoic acid (ALA) in the prevention and early treatment of CaOx deposition in rats. Sixty rats were divided into six groups (n=10 per group). Ethylene glycol (EG) and ammonium chloride (AC) (0.75% EG + 0.75% AC) were added to the drinking water of different groups for 7 or 14 days to induce nephrolithiasis. The effects of the CaOx and ALA (100 mg/kg per day orally) on kidney were investigated via histopathological, immunohistochemical, and biochemical methods. EG+AC application for both 7 and 14 days caused crystal accumulation in the tubule lumens, cystically dilated tubules, and hydropic degeneration in the tubular epithelium. However, inflammatory cell infiltration was observed merely in 14 days. When EG+AC administration was applied for 14 days only, it caused expression of ED1, alpha smooth muscle actin (alpha-SMA), and vimentin in the tubulointerstitial areas. However, alpha-SMA and vimentin expression was not observed in tubular epithelial cells. Transforming growth factor beta-1 (TGF-01) expression was also detected in the tubules and intertubular cells at 14 days. It was determined that ALA administration with EG+AC reduced the crystal accumulation in the tubule lumens (p<0.001), the degeneration of the tubular epithelium (p<0.001), and the expression of TGF-01. In addition, it was de- tected that ALA caused an increase in glutathione peroxidase (GPx) (p<0.001) and Catalase (CAT) (p>0.05) activities, which decreased with EG+AC application. This study suggests that ALA may be an effective strategy for reducing acute kidney injury caused by CaOx.eninfo:eu-repo/semantics/openAccessAlpha lipoic acidCalcium oxalateEpithelial Mesenchymal TransitionNephrolithiasisArticle7435911592010.12681/jhvms.288022-s2.0-85175189637Q4WOS:001089868200002Q4