LAUSR

Dexamethasone is a synthetic glucocorticoid that has been associated with oxidative stress in central and peripheral tissues. p-Chloro-diphenyl diselenide (p-ClPhSe)2 is an antioxidant organoselenium compound. The present study aimed to evaluate whether Nrf2/Keap-1 signaling contributes to the (p-ClPhSe)2 antioxidant effects in the kidney of mice exposed to dexamethasone. Adult Swiss mice received dexamethasone (i.p) at a dose of 2 mg/kg or its vehicle for 21 days. After, mice were treated with (p-ClPhSe)2 (i.g)(1, 5, or 10 mg/kg) for 7 days. Samples of kidneys were collected for biochemical assays. (p-ClPhSe)2 at dose of 1 mg/kg reversed the renal reactive oxygen species (ROS) and carbonyl protein (CP) levels increased by dexamethasone. (p-ClPhSe)2 at doses of 5 and 10 mg/kg was effective against the increase of TBARS (thiobarbituric acid reactive substances), ROS, and CP as well as the decrease of δ-aminolevulinic acid dehydratase (δ-ALA-D) activity and non-protein SH (NPSH) levels induced by dexamethasone. At 5 mg/kg, (p-ClPhSe)2 reduced the renal levels of 4-OH-2-HNE and HO-1 as well as modulated the Nrf2/Keap-1 signaling in mice exposed to dexamethasone. The present findings revealed that (p-ClPhSe)2 antioxidant effects were associated with the modulation of Nrf2/Keap-1 signaling pathway in the kidney of mice exposed to dexamethasone.