Melatonin protect the development of preimplantation mouse embryos from sodium fluoride-induced oxidative injury

被引:10
作者
Zhao, Jiamin [1 ,2 ]
Fu, Beibei [1 ,2 ]
Peng, Wei [1 ,2 ]
Mao, Tingchao [1 ,2 ]
Wu, Haibo [1 ,2 ]
Zhang, Yong [1 ,2 ]
机构
[1] Northwest A&F Univ, Coll Vet Med, Yangling 712100, Shaanxi, Peoples R China
[2] Northwest A&F Univ, Minist Agr, Key Lab Anim Biotechnol, Yangling 712100, Shaanxi, Peoples R China
基金
中国国家自然科学基金; 中国博士后科学基金;
关键词
Sodium fluoride; Melatonin; Antioxidant; Embryo; IN-VITRO; STRESS; MITOCHONDRIA; OOCYTES; ANTIOXIDANTS; ROLES;
D O I
10.1016/j.etap.2017.06.014
中图分类号
X [环境科学、安全科学];
学科分类号
08 ; 0830 ;
摘要
Recently study shows that melatonin can protect embryos from the culture environment oxidative stress. However, the protective effect of melatonin on the mouse development of preimplantation embryos under sodium fluoride (NaF) induced oxidative stress is still unclear. Here, we showed that exposure to NaF significantly increased the reactive oxygen species (ROS) level, decreased the blastocyst formation rates, and increased the fragmentation, apoptosis and retardation of blastocysts in the development of mouse preimplantation embryos. However, the protective of melatonin remarkable increased the of blastocyst formation rates, maintained mitochondrial function and total antioxidant capacity by clearing ROS. Importantly the data showed that melatonin improved the activity of enzymatic antioxidants, including glutathione(GSH), superoxide dismutase(SOD), and malonaldehyde (MDA), and increased the expression levels of antioxidative genes. Taken together, our results indicate that melatonin prevent NaF-induced oxidative damage to mouse preimplantation embryo through down regulation of ROS level, stabilization of mitochondrial function and modulation of the activity of antioxidases and antioxidant genes.
引用
收藏
页码:133 / 141
页数:9
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