The potential effect of methylseleninic acid (MSA) against γ-irradiation induced testicular damage in rats: Impact on JAK/STAT pathway.

Autor: Gawish RA; Drug Radiation Research Department, National Center for Radiation Research and Technology (NCRRT), Atomic Energy Authority, Cairo, Egypt. Electronic address: raniagawishbio86@yahoo.com., Fahmy HA; Drug Radiation Research Department, National Center for Radiation Research and Technology (NCRRT), Atomic Energy Authority, Cairo, Egypt., Abd El Fattah AI; Department of Biochemistry, Faculty of Pharmacy (Girls), Al-Azhar University, Cairo, Egypt., Nada AS; Drug Radiation Research Department, National Center for Radiation Research and Technology (NCRRT), Atomic Energy Authority, Cairo, Egypt.
Jazyk: angličtina
Zdroj: Archives of biochemistry and biophysics [Arch Biochem Biophys] 2020 Jan 15; Vol. 679, pp. 108205. Date of Electronic Publication: 2019 Nov 20.
DOI: 10.1016/j.abb.2019.108205
Abstrakt: This study suggested that methylseleninic acid (MSA) could respond to the inflammatory signaling associated with ionizing radiation-induced testicular damage. Mature male rats were divided into four groups: negative control, whole body γ-irradiated (IRR) (5 Gy), MSA (0.5 mg/kg, daily for nine consecutive days), and MSA+ IRR groups. MSA increased serum testosterone level and testicular glutathione peroxidase (GPx) as well as decreased the percentage of sperm abnormalities. Radiation prompted inflammatory signaling in the testes through increasing phospho-janus kinase1 (p-JAK1), phospho-signal transducers and activators of transcription 3 (p-STAT3) protein expressions. This induced increment in the inflammatory markers including nuclear factor- kappa B (NF-κB) and interleukin-1beta (IL-1β) levels. Also, radiation induced elevation of nitric oxide (NO) and malondialdhyde (MDA) levels with consequent reduction in testicular reduced glutathione level (GSH) and superoxide dismutase (SOD) activity. MSA significantly counteracted the radiation effect on testicular nuclear factor erythroid-2-related factor-2 (Nrf2) and suppressor of cytokine signaling (Socs3) protein expressions. In summary, this investigation proposed that MSA preserved spermatogenesis through increasing testosterone levels and GPx activity. Additionally, it diminished testicular inflammation by increasing of Nrf2 and Socs3 levels leading to reducing of p-JAK1, p-STAT3 and NF-κB levels. Histopathological examination results of testicular tissues showed a coincidence with the biochemical analysis.
(Copyright © 2019 Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
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