Protective activity of glutamine against bisphenol A-induced nephrotoxicity in rats

Bisphenol A (BPA) can impair kidney function via oxidative stress. Glutamine (Gln) is an amino acid with antioxidant and immunomodulatory activities. This study assessed the protective activity of Gln against BPA-induced nephrotoxicity in rats.

Thirty adult male Wistar rats (200-230g) were randomly divided into 6 groups (each containing 5 rats). The rats were orally treated daily for 60 days as follows: Groups A (Control), B, and C were treated with normal saline (0.2 mL), Gln (80 mg/kg), and BPA (50 mg/kg), respectively. Groups D-F were supplemented with 20 mg/kg, 40 mg/kg, and 80 mg/kg of Gln before treatment with BPA (50 mg/kg), respectively. Blood samples were collected and serum renal biochemical markers were measured. The kidneys were weighed and evaluated for oxidative stress markers and histological changes.

Administration of BPA decreased body weight (p<0.01) and increased kidney weight (p<0.01) when compared with the control group. The BPA-induced alterations in serum renal biochemical markers were accompanied by elevated urea (p<0.001), creatinine (p<0.001), and uric acid levels (p<0.001) as well as decreased electrolytes (p<0.01) when compared with the control group. Altered kidney oxidative stress markers caused by BPA were marked by a significant decrease in glutathione, catalase, superoxide dismutase and glutathione peroxidase levels (p<0.001) with a significant increase in malondialdehyde levels (p<0.001) compared with the control group. Moreover, BPA caused kidney tubular necrosis, widened bowman’s space, collapsed glomerulus, and lipid accumulation. However, supplementation with Gln (20, 40, and 80 mg/kg) significantly reversed the BPA-induced nephrotoxicity in a dose-dependent manner compared with the BPA group. Furthermore, different doses of Gln restored kidney histology.

Based on the results, Gln may have clinical protective effects against BPA-associated nephrotoxicity.