Role of peroxiredoxin 2 in H2O2-induced oxidative stress of primary Leydig cells

Abstract

Late‑onset hypogonadism is defined as a condition caused by a decline in the levels of testosterone with aging. One of the major factors contributing to the low levels of testosterone is the accumulation of reactive oxygen species (ROS) in Leydig cells during the ageing process. Peroxiredoxin 2 (Prdx2), a member of the peroxiredoxin family, is an antioxidant protein, the predominant function of which is to neutralize ROS. However, its role in Leydig cells remains to be elucidated. In the present study, primary Leydig cells were exposed to low concentrations of hydrogen peroxide (H2O2) to induce oxidative stress. Cell apoptosis was measured using an Annexin V fluorescein isothiocyanate/propidium iodide apoptosis detection kit and flow cytometry. The level of testosterone was determined by radioimmunoassay, and the mRNA and protein expression levels of Prdx2 were detected by reverse transcription‑polymerase chain reaction and western blotting, respectively. The results revealed a significant increase in cell apoptosis and decrease in testosterone production. In addition, the expression of Prdx2 was decreased by H2O2 in a dose‑ and time‑dependent manner, and this decrease may have been caused by the induction of its molecular structure transformation due to H2O2 elimination. The above findings indicated that Prdx2 may prevent H2O2 accumulation in Leydig cells, and may be important in oxidative stress‑induced apoptosis and decreased testosterone production.

Mechanistic Role of Reactive Oxygen Species and Therapeutic Potential of Antioxidants in Denervation- or Fasting-Induced Skeletal Muscle Atrophy

“…Sirt2, 3 and 5 decreases the cellular levels of ROS or promotes the transcription of manganese superoxide dismutase (MnSOD) (Wang et al, 2007 ; Lin et al, 2013 ; Pillai et al, 2016 ; Yang et al, 2016 ). Pink1 overexpression could suppress ROS formation, and Prdx2 is an antioxidant protein, whose predominant function is to neutralize ROS (Wang et al, 2011 ; Chien et al, 2013 ; Avitabile et al, 2014 ; Duan et al, 2016 ). Therefore, down-regulation of above identified genes (cataloged into class 2) during denervation-induced skeletal muscle atrophy might be due to their function as a negative regulator of ROS production.…”

Effects of saturated palmitic acid and omega-3 polyunsaturated fatty acids on Sertoli cell apoptosis

“…Total RNA extraction and qPCR were carried out as described previously (Duan et al 2016). The primer sequences (synthesized by Shanghai Generay Biotech Co., Ltd., Shanghai, China) were as follows: sense 3ʹgaaactgctgcctcacatccg-5ʹ and anti-sense 3ʹ-gctggcacagtgacctcacacg-5ʹ for acidic ribosomal phosphoprotein P0 (36B4); sense 3ʹ-cagcagcccatgaattaccc-5ʹand anti-sense 3ʹ-caccggtagccacagatttg-5ʹ for FasL; and sense 3ʹ-agacatgctgtggatctggg-5ʹ and anti-sense 3ʹ-ttgacagcaaaatgggcctc-5ʹ for Fas.…”

“…Western blot analysis was performed as described previously (Duan et al 2016). Briefly, following treatment, cells in a 6 cm cell culture dish were then washed twice with ice-cold PBS and lysed in 150 µl of ice-cold radioimmunoprecipitation assay buffer (RIPA, Sigma, America) for 10 min on the ice.…”

Silencing of PRDX2 Inhibits the Proliferation and Invasion of Non-Small Cell Lung Cancer Cells

“…Previous studies have shown that one of the known mechanisms of carcinogenesis is the activation of various signaling pathways and changes of transcription factors caused by prolonged oxidative stress [12,13]. As a key member of PRDXs family, peroxiredoxin 2 (PRDX2) has been reported to scavenge peroxides and reactive oxygen species (ROS) in cells to regulate redox status, thus participating in a variety of cellular biological functions [14][15][16]. Recent studies identify aberrant expression of PRDX2 in several types of cancers and demonstrate that PRDX2 exerts an important role in cell proliferation, death, and drug sensitivity of cancer [17][18][19][20].…”