硒蛋白
氧化损伤
氧化磷酸化
细胞生物学
化学
硒蛋白P
基因表达
氧化应激
生物
生物化学
解剖
基因
过氧化氢酶
谷胱甘肽过氧化物酶
作者
Yixin Cui,Yucheng Liao,Yonghui Chen,Xu Zhao,Yi Zhang,Hui Wang,Lian Li,Xinhe Zhang,Kunpan Chen,Mingzhao Jia,Jing Tian,Xingran Ruan,Yawen Shi,Pinglin Yang,Jinghong Chen
标识
DOI:10.1016/j.jtemb.2024.127492
摘要
Low levels of the indispensable trace element selenium (Se) can cause oxidative stress and disrupt environmental homeostasis in humans and animals. Selenoprotein S (Selenos), of which Se is a key component, is a member of the selenoprotein family involved in various biological processes. This study aimed to investigate whether low-level SELENOS gene expression can induce oxidative stress and decrease the antioxidative capacity of chondrocytes. Compared with control cells, SELENOS-knockdown ATDC5 cells showed substantially higher dihydroethidium, reactive oxygen species and malondialdehyde levels, and lower superoxide dismutase (SOD) expression. Knockout of the gene in C57BL/6 mice increased the 8-hydroxy-2-deoxyguanosine level considerably and decreased SOD expression in cartilages relative to the levels in wild-type mice. The results showed that the increased nuclear factor erythroid 2-related factor 2/heme oxygenase-1 signaling mediated by low-level SELENOS expression was involved in oxidative damage. The proliferative zone of the cartilage growth plate of SELENOS-knockout mice was shortened, suggesting cartilage differentiation dysfunction. In conclusion, this study confirmed that low-level Selenos expression plays a role in oxidative stress in cartilages.
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