The Effects of Selenium in Acrylamide-Induced Nephrotoxicity in Rats: Roles of Oxidative Stress, Inflammation, Apoptosis, and DNA Damage

• Published in: Biological trace element research 2021, Vol.199 (1), p.173-184
• Main Authors: Sengul, Emin, Gelen, Volkan, Yildirim, Serkan, Tekin, Samet, Dag, Yusuf
• Format: Article
• Language: English
• Subjects: 8-Hydroxydeoxyguanosine; Acrylamide; Anaesthesia; Anesthesia; Apoptosis; BAX protein; Biochemistry; Biomedical and Life Sciences; Biotechnology; Blood; Caspase-3; Catalase; Creatinine; Cyclooxygenase-2; Damage; Deoxyguanosine; Deoxyribonucleic acid; DNA; DNA damage; ELISA; Enzyme-linked immunosorbent assay; Glutathione; Glutathione peroxidase; Histopathology; IL-1β; Inflammation; Interleukin 6; Kidneys; Kinases; Life Sciences; Malondialdehyde; MAP kinase; Necrosis; Neoplasms; NF-κB protein; Nutrition; Oncology; Oxidative stress; Peroxidase; Protein kinase; Rodents; Selenium; Serum; Superoxide dismutase; Tissue; Tumor necrosis factor-TNF; Tumor necrosis factor-α; Urea
• ISSN: 0163-4984; 1559-0720
• DOI: 10.1007/s12011-020-02111-0

We sought to determine the effects of selenium (Se) on acrylamide (ACR)-induced nephrotoxicity in rats. In our study, 50 adult male Sprague-Dawley rats weighing 200–250 g were randomly divided into five groups. The control group was given intra-gastric (i.g.) saline (1 mL) for 10 days. The ACR group was given i.g. ACR in saline (38.27 mg/kg titrated to 1 mL) for 10 days. The Se0.5 + ACR and Se1 + ACR groups were administered Se in saline (0.5 and 1 mg/kg, respectively) for 10 days and given i.g. ACR (38.27 mg/kg) one hour after the Se injections. The Se1 group was administered i.g. Se (1 mg/kg) for 10 days. On day 11, intracardiac blood samples were obtained from the rats while they were under anesthesia, after which they were euthanized by decapitation. Urea and creatinine concentrations of blood serum samples were analyzed with an autoanalyzer. Enzyme-linked immunosorbence immunosorbent assay (ELISA) was used to quantify malondialdehyde (MDA), superoxide dismutase (SOD), glutathione (GSH), glutathione peroxidase (GPx), catalase (CAT), tumor necrosis factor-α (TNF-α), nuclear factor-κB (NF-κB), interleukin (IL)-33, IL-6, IL-1β, cyclooxygenase-2 (COX-2), kidney injury molecule-1 (KIM-1), mitogen-activated protein kinase-1 (MAPK-1), and caspase-3 in kidney tissues. Renal tissues were evaluated by histopathological and immunohistochemical examinations for 8-hydroxylo-2′-deoxyguanosin 8-hydroxy-2′-deoxyguanosine (8-OhDG) and Bax. Serum urea and creatinine levels were higher in the ACR group than in the control, and these ACR-induced increases were prevented by high doses of Se. Additionally, ACR induced the renal oxidative stress, inflammation, apoptosis, and damage to DNA and tissue; likewise, these were prevented by high doses of Se. Taken with ACR, Se confers protection against ACR-induced nephrotoxicity in rats by reducing oxidative stress, inflammation, apoptosis, and DNA damage.