Human exposure to sodium fluoride through its daily usage is almost inevitable. Cardiovascular and renal dysfunction has been associated with fluoride toxicity. Therefore, this study investigated the mechanism of action of sodium fluoride (NaF) induced hypertension and cardiovascular complications Forty male albino rats of an average of 10 rats per group were used. Group A received clean tap water. Toxicity was induced in Group B to D by administering graded doses of NaF through drinking water ad libitum for 10 days at 150 ppm, 300 ppm, and 600 ppm concentration respectively. Following administration of NaF, there was significant increase in systolic pressure, diastolic pressure and mean arterial pressure. Markers of oxidative stress; malondialdehyde, hydrogen peroxide, advance oxidation protein products, and protein carbonyl were significantly increased in dose‐dependent pattern in the cardiac and renal tissues of rats together with significant decrease in the GST activity in NaF‐treated rats compared to the control. Also serum markers of inflammation, cardiac, and renal damage including myeloperoxidase, xanthine oxidase, blood urea nitrogen, creatinine, Lactate dehydrogenase (LDH), and Creatinine kinase myocardial band (CK‐MB) significantly increased indicating induction of oxidative stress, renal, and cardiac damage after exposure. Histopathology of the kidney and heart revealed aberrations in the histological architecture in NaF‐treated rats. Also, immunohistochemistry showed higher expression of nuclear factor kappa beta (NF‐kB) in the cardiac and renal tissues of rats administered NaF. Combining all, these results indicate NaF‐induced hypertension through generation of reactive oxygen species and activation of renal and cardiac NF‐kB expressions. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 1089–1101, 2017.

中文翻译：

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氟化钠通过产生活性氧和激活核因子κβ诱导高血压和心脏并发症

人类通过日常使用接触氟化钠几乎是不可避免的。心血管和肾功能障碍与氟化物毒性有关。因此，本研究调查了氟化钠 (NaF) 诱发的高血压和心血管并发症的作用机制，使用了 40 只雄性白化大鼠，平均每组 10 只。A 组接受干净的自来水。在 B 至 D 组中，通过分别以 150 ppm、300 ppm 和 600 ppm 的浓度通过饮用水随意施用分级剂量的 NaF 10 天来诱导毒性。NaF 给药后，收缩压、舒张压和平均动脉压显着升高。氧化应激的标志物；丙二醛、过氧化氢、高级氧化蛋白产品、与对照组相比，NaF 治疗的大鼠的心脏和肾脏组织中，羰基和蛋白质的剂量依赖性显着增加，同时 GST 活性显着降低。炎症、心脏和肾脏损伤的血清标志物，包括髓过氧化物酶、黄嘌呤氧化酶、血尿素氮、肌酐、乳酸脱氢酶 (LDH) 和肌酐激酶心肌带 (CK-MB) 显着增加，表明诱导氧化应激、肾脏和暴露后心脏受损。肾脏和心脏的组织病理学揭示了 NaF 治疗大鼠的组织学结构异常。此外，免疫组织化学显示，在给予 NaF 的大鼠的心脏和肾脏组织中，核因子 kappa β (NF-kB) 的表达更高。综合所有，这些结果表明 NaF 通过产生活性氧和激活肾脏和心脏 NF-kB 表达引起高血压。© 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 1089–1101, 2017。