Vitamin C Attenuates Sodium Fluoride-Induced Mitochondrial Oxidative Stress and Apoptosis via Sirt1-SOD2 Pathway in F9 Cells.

Vitamin C Attenuates Sodium Fluoride-Induced Mitochondrial Oxidative Stress and Apoptosis via Sirt1-SOD2 Pathway in F9 Cells. Biol Trace Elem Res. 2018 Dec 18;: Authors: Peng W, Xu S, Zhang J, Zhang Y Abstract Increasing evidence has suggested an important role played by reactive oxygen species (ROS) in the pathogenesis of fluorosis. Accumulating evidence demonstrates that vitamin C administration ameliorate sodium fluoride (NaF)-induced oxidative stress. However, the potentially beneficial effects of vitamin C against NaF-induced cytotoxicity and the underlying molecular mechanisms of this protection are not fully understood. Here, we found that NaF stimulated cytotoxicity, increased mitochondrial reactive oxygen species (mROS) production, and induced apoptosis in F9 embryonic carcinoma cells. Consistent with this finding, NaF exposure was associated with decreased Sirtuin 1 (Sirt1) protein expression, thus promoted the acetylation of manganese superoxide dismutase (SOD2), a key enzyme involved in regulating mROS production. However, all NaF-induced mitochondrial oxidative injuries were efficiently ameliorated by overexpression of Sirt1 or incubation with Mito-TEMPO (a SOD2 mimetic). Moreover, pretreatment with vitamin C enhanced the expression of Sirt1 and decreased NaF-induced mitochondrial oxidative stress and apoptosis. Knockdown of Sirt1 blocked the vitamin C-mediated reduction in mROS and apoptosis via inhibiting Sirt1-SOD2 si...
Source: Biological Trace Element Research - Category: Biology Authors: Tags: Biol Trace Elem Res Source Type: research