Gum Arabic Mitigates AlCl3-Induced Nephrotoxicity by Upregulating the XRCC1 Gene and Downregulating Ki67 and P53 Expressions

The kidney is an important organ for the elimination of waste products. However, insults to the kidney arising from the effects of reactive oxygen species could limit its functions. This study evaluated the nephroprotective effects of Gum Arabic, an FDA-approved edible fiber against aluminum chloride (AlCl3)-induced nephrotoxicity in rats and its impact on XRCC1 gene expression and Ki67 and p53 immunoreactivity. Twenty male Wistar rats were divided into four groups of five (n = 20). In Group 1, there was no intervention for the control group. A 5-mg/kg intraperitoneal (IP) AlCl₃ dosage was administered to Group 2 throughout a 2-week period. Gum Arabic (GA) extract was administered orally to Group 3 for 4 weeks at a dose of 500 mg/kg body weight. Group 4 received an IP dose of AlCl₃ at 5mg/kg body weight for 2 weeks followed by a 500 mg/ kg body weight oral dose of GA extract for 4 weeks. The following variables were evaluated: body weight, relative kidney weight, serum urea, uric acid, tissue oxidative stress, ERCC1 gene expression, kidney histology, and Ki67 and p53 immunoreactivity. The findings demonstrated that giving rats AlCl3 reduced the amount of SOD, and GSH in their kidneys and caused alteration in the kidney tissue histoarchitecture, while also increasing the serum levels of urea, tissue lipid peroxidation, and Ki67 and p53 positive immunoreactivity. Interestingly, GA treatment following AlCl3 administration to rats mitigated these changes. Taken together, this study showed the capacity of Gum Arabic as a nephroprotective agent against AlCl3-induced nephrotoxicity.