Chronic Exposure to Sodium Arsenite Alters the Expression of Renin–Angiotensin System, Apoptosis and Oxidative Stress Markers in Wistar Rat

The renin–angiotensin system (RAS) of the kidney is responsible for renal regulation and homeostasis, and patients with chronic kidney disease frequently receive RAS blockades. The purpose of this study was to determine the connection between the stimulation of arsenic in rats and changes in transcription levels of RAS hormones, biochemical parameters and antioxidant enzymes. Twenty-five Wistar rats were divided into five groups (control, low, middle, high dose and high dose + a-tocopherol groups) and given oral doses of 8.2, 12.3 and 16.4 mg/kg sodium arsenite (NaAsO₂) and 50 mg/kg a-toco­pherol for two months. RT-PCR analysis in nephrocytes revealed that mRNA expression of p53, p21, p27, caspases (3, 7 and 9), ACE, AGT, AT1R, CYP1A1 and Bax was found to be upregulated by ~1.9, ~1.6, ~1.5, ~2.3, ~3.3, ~3, ~2, ~1.9, ~2.4, ~1.7 and ~3.3-fold, whereas that of cyclin A, cyclin B1, cyclin E1, CDK 1, CDK 2, Bcl-2, CAT, SOD, GPx, GR and GST was downregulated consistently in renal tissues of arsenic-exposed groups by ~0.6, ~0.5, ~0.4, ~0.5, ~0.6, ~0.5, ~0.6, ~0.4, ~0.6, ~0.5 and ~0.6-fold respectively. The acti­vities of alkaline phosphatase, acid phosphatase and antioxidant enzymes were significantly reduced by 63%, 71%, 40%, 37% and 44% respectively, upon treatment with NaAsO2. Through this study, we can gain knowledge about the potential function of RAS enzymes and antioxidant enzymes against the detrimental effects of arsenic-induced oxidative stress due to altered transcription levels of RAS enzymes in Wistar rats.