Journal
MOLECULAR BIOLOGY REPORTS
Volume 46, Issue 6, Pages 6155-6164Publisher
SPRINGER
DOI: 10.1007/s11033-019-05050-9
Keywords
Acute fluoride toxicity; Cardiac dysfunction; Inflammation; NF-kappa B activation; Redox signaling
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Funding
- Indian Council of Medical Research, New Delhi [45/25/2013/BMS/TRM]
- UGC-BSR, New Delhi, India [F7-25/2007]
- University Grants Commission-Special Assistance Programme [UGC-SAP-II:F-3-20/2013]
- Department of Science and Technology, Fund for Improvement of Science and Technology infrastructure in universities and higher educational institutions, New Delhi, India [DST-FIST:SR/FST/LSI-618/2014]
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Acute fluoride (F-) exposure adversely impairs cardiac functions. We previously reported that acute F- toxicity causes modulation in oxidant and antioxidant systems, heat shock proteins, cytoskeletal proteins and AMPK signaling proteins in the myocardium of rats. With these findings, we hypothesized that acute F- intoxication may trigger an acute myocardial inflammatory response through the activation of NF-kappa B signaling and reduction of redox signaling regulatory system. To test this hypothesis, we treated male Wistar rats with single oral doses of 45 and 90 mg/kg of F- for 24 h. The myocardium of F- treated rats showed increased expression of pNF-kappa B, pI kappa K alpha/beta eventually leading to the increased expression of downstream target TNF alpha-a major proinflammatory cytokine secreted in the inflammatory process. F- intoxication decreased the mRNA expression of redox genes-Sirt1, Sirt3, Prdx2, Glrx1, Trx1, and Trx2. In addition, we observed decreased protein expression of Nrf2, GCLC, and NQO1 in the cardiac tissues of F- treated rats. This study reveals that F- toxicity triggers myocardial inflammatory response and depletes redox signaling molecules in the myocardium of rats. We conclude that NF-kappa B activation with decreased redox gene expression might be associated with the pathophysiology of F- induced cardiac dysfunction in rats. This finding provides new insights into the cardiovascular pathophysiology in acute F- toxicity.
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