Abstract

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 200-250g were randomly divided into five groups. The control group was given intra-gastric (i.g.) saline (1mL) for 10days. The ACR group was given i.g. ACR in saline (38.27mg/kg titrated to 1mL) for 10days. The Se0.5 + ACR and Se1 + ACR groups were administered Se in saline (0.5 and 1mg/kg, respectively) for 10days and given i.g. ACR (38.27mg/kg) one hour after the Se injections. The Se1 group was administered i.g. Se (1mg/kg) for 10days. 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 immunosorbenceimmunosorbent 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.

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