氧化应激
过氧化氢酶
细胞毒性
化学
活性氧
细胞凋亡
非西汀
地塞米松
活力测定
药理学
超氧化物歧化酶
一氧化氮
成骨细胞
内分泌学
内科学
抗氧化剂
生物化学
类黄酮
生物
医学
体外
有机化学
作者
Iwona Inkielewicz‐Stępniak,Marek W. Radomski,Marek W. Radomski
标识
DOI:10.1016/j.fct.2011.12.015
摘要
Fluoride intoxication and dexamethasone treatment produce deleterious effects in bone and brain. The aim of this study was to evaluate the effect of fluoride (F) and dexamethasone (Dex) co-exposure on oxidative stress and apoptosis in osteoblast-like MC3T3-E1 and hippocampal HT22 cell lines. Co-exposure to F and Dex resulted in a concentration-dependent decrease in cell viability, induction of apoptosis and increased generation of reactive oxygen species (ROS) and nitric oxide (NO) following 72 h of incubation. Fluoride-induced apoptosis in MC3T3-E1 and HT22 cells was attenuated by catalase and L-NNMA, indicating a role for H2O2 and NO as mediators of cytotoxicity. Dexamethasone-induced apoptosis was associated with H2O2 generation in both cell lines and it was attenuated during co-incubation with catalase. These data indicate that co-exposure to F and Dex amplifies their respective cytotoxicity in H2O2- and NO-dependent manner. As flavonoid fisetin prevented F- and Dex-induced cytotoxicity the potential role of this product in pharmacology and diet may be considered.
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