Sodium fluoride induces hypertension and cardiac complications through generation of reactive oxygen species and activation of nuclear factor kappa beta

Abstract

Human exposure to sodium fluoride through daily use is almost inevitable, and fluoride toxicity has been associated with cardiovascular and renal dysfunction. This study investigated the mechanism of sodium fluoride (NaF)-induced hypertension and cardiovascular complications using forty male albino rats divided into four groups of ten rats each. Group A received clean tap water, while Groups B to D received graded doses of NaF in drinking water ad libitum for 10 days at concentrations of 150 ppm, 300 ppm, and 600 ppm respectively. NaF administration caused significant increases in systolic pressure, diastolic pressure, and mean arterial pressure. Markers of oxidative stress, including malondialdehyde, hydrogen peroxide, advanced oxidation protein products, and protein carbonyl, increased significantly in a dose-dependent manner in cardiac and renal tissues, alongside a significant decrease in GST activity compared to the control group. Serum markers of inflammation, cardiac injury, and renal damage such as myeloperoxidase, xanthine oxidase, blood urea nitrogen, creatinine, lactate dehydrogenase (LDH), and creatinine kinase myocardial band (CK-MB) were also significantly elevated, indicating oxidative stress as well as renal and cardiac damage after exposure. Histopathological examination of the kidney and heart revealed abnormalities in tissue architecture in NaF-treated rats, while immunohistochemistry demonstrated increased expression of nuclear factor kappa beta (NF-kB) in cardiac and renal tissues. Overall, the findings indicate that NaF induces hypertension through the generation of reactive oxygen species and activation of renal and cardiac NF-kB expression