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Environ Toxicol. 2017 Apr;32(4):1089-1101. doi: 10.1002/tox.22306. Epub 2016 Jul 5.

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

Author information

1
Department of Veterinary Physiology, Biochemistry and Pharmacology, Faculty of Veterinary Medicine, University of Ibadan, Nigeria.
2
Department of Veterinary Medicine, Faculty of Veterinary Medicine, University of Ibadan, Nigeria.
3
Department of Veterinary Biochemistry, Faculty of Veterinary Medicine, University of Benin, Nigeria.
4
Department of Environmental and Interdisciplinary Sciences, College of Science, Technology and Engineering, Texas Southern University, 3100 Cleburne Avenue, Houston, TX, 77004, USA.

Abstract

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.

KEYWORDS:

NF-kB; ROS; cardiovascular complications; hypertension; sodium fluoride

PMID:
27378751
DOI:
10.1002/tox.22306
[Indexed for MEDLINE]

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