p -Chloro-diphenyl diselenide modulates Nrf2/Keap1 signaling and counteracts renal oxidative stress in mice exposed to repeated dexamethasone administrations

Dexamethasone is a synthetic glucocorticoid that has been associated with oxidative stress in central and peripheral tissues. p-Chloro-diphenyl diselenide ([(p-ClPhSe).sub.2]) is an antioxidant organoselenium compound. The present study evaluated whether nuclear factor (erythroid-derived 2)-like 2 (...

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Published in:Canadian journal of physiology and pharmacology 2022-06, Vol.100 (6), p.500-508
Main Authors: Muller, Sabrina G, Heck, Suelen O, Marques, Luiza S, Zborowski, Vanessa A, Nogueira, Cristina W
Format: Article
Language:English
Subjects:
Aminolevulinic acid
Antioxidants
Carbonyl compounds
Care and treatment
Causes of
Cellular signal transduction
Complications and side effects
Dexamethasone
Glucocorticoids
Health aspects
Heme
Kidney diseases
Kidneys
Oxidative stress
Oxygenase
Reactive oxygen species
Selenides
Signal transduction
Steroids
Thiobarbituric acid
Thiols
Transcription factors
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Summary:Dexamethasone is a synthetic glucocorticoid that has been associated with oxidative stress in central and peripheral tissues. p-Chloro-diphenyl diselenide ([(p-ClPhSe).sub.2]) is an antioxidant organoselenium compound. The present study evaluated whether nuclear factor (erythroid-derived 2)-like 2 (Nrf2)/Kelch-like ECH-associated protein 1 (Keap-1) signaling contributes to the [(p-ClPhSe).sub.2] antioxidant effects in the kidney of mice exposed to dexamethasone. Adult Swiss mice received dexamethasone (intraperitoneal) at a dose of 2 mg/kg or its vehicle for 21 days. After that, mice were treated with [(p- ClPhSe).sub.2] (intragastric) (1, 5, or 10 mg/kg) for 7 days. Samples of kidneys were collected for biochemical assays. [(p-ClPhSe).sub.2] at a dose of 1 mg/kg reversed the renal reactive oxygen species (ROS) and carbonyl protein (CP) levels increased by dexamethasone. [(p-ClPhSe).sub.2] at doses of 5 and 10 mg/kg was effective against the increase of thiobarbituric acid reactive substances, ROS, and CP, as well as the decrease of [delta]-aminolevulinic acid dehydratase activity and nonprotein sulfhydryl levels induced by dexamethasone. At 5 mg/kg, [(p-ClPhSe).sub.2] reduced the renal levels of 4-OH-2-HNE and heme oxygenase (HO-1), as well as modulated the Nrf2/Keap-1 signaling in mice exposed to dexamethasone. The present findings revealed that [(p-ClPhSe).sub.2] antioxidant effects were associated with the modulation of Nrf2/Keap-1 signaling pathway in the kidney of mice exposed to dexamethasone.
ISSN:0008-4212
1205-7541
DOI:10.1139/cjpp-2021-0573