• Modeling Mechanism：

  Glyfosfin, as a direct precursor to oxalate, is rapidly converted into oxalate in the body, causing a sharp increase in urinary oxalate concentration and resulting in hyperoxaluria. At the same time, it triggers oxidative stress in renal tubular epithelial cells (increased ROS and MDA, decreased SOD) and mitochondrial damage, promoting the nucleation and deposition of calcium oxalate (CaOx) crystals in the renal tubular lumen, accompanied by inflammatory infiltration and kidney damage, ultimately forming calcium oxalate kidney stones.

• Related Products：

  Glyfosfin (T21306)

• Modeling Method：

  Experimental Subject：

  Mice, ICR, Male, 25±3g, 6-8 weeks old

  Dosage and Administration Route：

  Glyfosfin, 100 mg/kg, saline, intraperitoneal injection (i.p.)

  Dosing Frequency and Duration Model：

  Once daily for 7 consecutive days

• Validation：

  1. Pathological gold standard: Under Pizzolato staining and polarized light microscopy, a large number of calcium oxalate crystal deposits were observed in the lumen of the renal tubules; under transmission electron microscopy, mitochondrial swelling and microvilli loss were observed in the renal tubular epithelial cells, and crystal nuclei were formed in the lumen; 2. Functional indicators: Serum creatinine (Cr) and blood urea nitrogen (BUN) were significantly elevated; the calcium and oxalate content in the renal tissue were significantly increased compared with the control group; 3. Oxidative stress: The levels of ROS and MDA in the renal tissue were elevated, the activity of SOD was decreased, and the expression of 4-HNE (a marker of lipid peroxidation) was upregulated.

*Precautions： The animal was sacrificed after the last dose on day 7, and its kidneys were rapidly separated.

*References：Khan SR, Glenton PA. Experimental induction of calcium oxalate nephrolithiasis in mice. J Urol. 2010 Sep;184(3):1189-96.