RETRACTED ARTICLE: Sulforaphane potentially attenuates arsenic-induced nephrotoxicity via the PI3K/Akt/Nrf2 pathway in albino Wistar rats

Sulforaphane Nephrotoxicity
DOI: 10.1007/s11356-019-04502-w Publication Date: 2019-03-05T10:54:08Z
ABSTRACT
Abstract Oxidative stress plays a significant role in the pathophysiology of numerous kidney diseases, generally mediated by reactive oxygen species (ROS). Arsenic (Ar) is known to exert its toxicity through generation ROS and inflammation. The current study investigates protective effects sulforaphane (SFN) against arsenic-induced renal damage via PI3K/Akt-mediated Nrf2 pathway signaling. Thirty-two male albino Wistar rats were randomly divided into four groups eight animals each, designated as control, arsenic (Ar), plus Ar (SFN+Ar), alone (SFN), with oral administration (5 mg/kg BW) SFN (80 daily for 28 days. significantly ( P < 0.05) increased levels ROS, OHdG, accumulation, lipid peroxidation, decreased enzymatic nonenzymatic antioxidants. Notably, increase was observed markers apoptosis, DNA damage, TUNEL-positive cells, dark staining ICAM-1 tissue PI3K/Akt/Nrf2 gene expression. biochemical findings supported histopathological electron microscopy evaluation, which showed severe treated Ar. Pretreatment attenuated phase II antioxidants activation tissue. These results show that dietary supplementation protects Ar-induced nephrotoxicity signaling rat kidney.
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