SOD2
SIRT3
线粒体
和厚朴酚
锡尔图因
活性氧
线粒体ROS
化学
TFAM公司
超氧化物歧化酶
氟化钠
细胞生物学
卵母细胞
药理学
氧化应激
生物
线粒体生物发生
生物化学
氟化物
乙酰化
胚胎
无机化学
基因
作者
Xin-Yue Qi,Jin-Dong Yuan,Ziyu Liu,Xi-Qing Jiang,Qi Zhang,Shan-Long Zhang,Lu Zhao,Ling-Yan Ke,Chen-Yuan Zhang,Yan Li,Zhang Lu-yan,Qianqian Xu,Liu Z,Jing‐Tao Sun,Jun‐Xue Jin
标识
DOI:10.1016/j.scitotenv.2023.168306
摘要
Fluoride exerts detrimental effects on germ cells and increases the infertility rate in women. Nevertheless, the precise mechanisms behind the developmental abnormalities caused by fluoride in oocytes remain poorly comprehended. The current study, we established mitochondrial damage model in oocytes via 50 μg/mL sodium fluoride (NaF) supplementation. We then examined the effects of honokiol in preventing mitochondrial deficits caused by NaF and investigated the mechanisms through which honokiol protects oocytes. The findings investigated that NaF increased levels of mitochondrial reactive oxygen species (mtROS) and hindered mitochondrial function, as evidenced by the dissipation of mitochondrial membrane potential, abnormal expression of mitochondrial DNA copy numbers, and mtDNA harm in oocytes. mtROS scavenging using Mito-TEMPO alleviated oxidative damage in mitochondria and restored the oocyte developmental competence. Superoxide dismutase 2 (SOD2) acetylation was significantly increased, whereas sirtuin 3 (SIRT3) expression was decreased in NaF-treated oocytes. The addition of honokiol helped in the deacetylation of SOD2 at K122 through SIRT3, resulting in the removal of excessive mtROS and the recovery of mitochondrial function. Therefore, SIRT3/SOD2 pathway aids honokiol in mitigating fluoride-induced mitochondrial dysfunction. Overall, honokiol improved the mitochondrial harm caused by NaF by controlling mtROS and mitochondrial function, with the SIRT3/SOD2 pathway having an important function. These findings suggest honokiol as a potential therapeutic strategy for NaF-induced oocyte development and mitochondrial deficits.
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