دوره 6، شماره 3 - ( 9-1401 )
جلد 6 شماره 3 صفحات 26-23 |
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Ehigiator E B, Adikwu E, Chiwendu Ifeduba A. Protective activity of glutamine against bisphenol A-induced nephrotoxicity in rats. jcbr 2022; 6 (3) :23-26
URL: http://jcbr.goums.ac.ir/article-1-375-fa.html
URL: http://jcbr.goums.ac.ir/article-1-375-fa.html
Protective activity of glutamine against bisphenol A-induced nephrotoxicity in rats. Journal of Clinical and Basic Research. 1401; 6 (3) :23-26
چکیده: (1214 مشاهده)
Background and objectives: 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.
Methods: 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.
Results: 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.
Conclusion: Based on the results, Gln may have clinical protective effects against BPA-associated nephrotoxicity.
Methods: 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.
Results: 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.
Conclusion: Based on the results, Gln may have clinical protective effects against BPA-associated nephrotoxicity.
نوع مقاله: پژوهشي |
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علوم پایه پزشکی
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