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Oyagbemi AA, Adejumobi OA, Jarikre TA, et al. Clofibrate, a Peroxisome Proliferator-Activated Receptor-Alpha (PPARα) Agonist, and Its Molecular Mechanisms of Action against Sodium Fluoride-Induced Toxicity. Biol Trace Elem Res. 2021;doi: 10.1007/s12011-021-02722-1.
Oyagbemi, A. A., Adejumobi, O. A., Jarikre, T. A., Ajani, O. S., Asenuga, E. R., Gbadamosi, I. T., Adedapo, A. D. A., Aro, A. O., Ogunpolu, B. S., Hassan, F. O., Falayi, O. O., Ogunmiluyi, I. O., Omobowale, T. O., Arojojoye, O. A., Ola-Davies, O. E., Saba, A. B., Adedapo, A. A., Emikpe, B. O., Oyeyemi, M. O., Nkadimeng, S. M., McGaw, L. J., Kayoka-Kabongo, P. N., Oguntibeju, O. O., & Yakubu, M. A. (2021). Clofibrate, a Peroxisome Proliferator-Activated Receptor-Alpha (PPARα) Agonist, and Its Molecular Mechanisms of Action against Sodium Fluoride-Induced Toxicity. Biological trace element research, . https://doi.org/10.1007/s12011-021-02722-1
Oyagbemi, Ademola Adetokunbo, et al. "Clofibrate, a Peroxisome Proliferator-Activated Receptor-Alpha (PPARα) Agonist, and Its Molecular Mechanisms of Action against Sodium Fluoride-Induced Toxicity." Biological trace element research vol. (2021). doi: https://doi.org/10.1007/s12011-021-02722-1
Oyagbemi AA, Adejumobi OA, Jarikre TA, Ajani OS, Asenuga ER, Gbadamosi IT, Adedapo ADA, Aro AO, Ogunpolu BS, Hassan FO, Falayi OO, Ogunmiluyi IO, Omobowale TO, Arojojoye OA, Ola-Davies OE, Saba AB, Adedapo AA, Emikpe BO, Oyeyemi MO, Nkadimeng SM, McGaw LJ, Kayoka-Kabongo PN, Oguntibeju OO, Yakubu MA. Clofibrate, a Peroxisome Proliferator-Activated Receptor-Alpha (PPARα) Agonist, and Its Molecular Mechanisms of Action against Sodium Fluoride-Induced Toxicity. Biol Trace Elem Res. 2021 Apr 24; doi: 10.1007/s12011-021-02722-1. Epub 2021 Apr 24. PMID: 33893992.
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Biol Trace Elem Res. 2021 Apr 24; doi: 10.1007/s12011-021-02722-1. Epub 2021 Apr 24.

Clofibrate, a Peroxisome Proliferator-Activated Receptor-Alpha (PPARα) Agonist, and Its Molecular Mechanisms of Action against Sodium Fluoride-Induced Toxicity.

Biological trace element research

Ademola Adetokunbo Oyagbemi, Olumuyiwa Abiola Adejumobi, Theophilus Aghogho Jarikre, Olumide Samuel Ajani, Ebunoluwa Racheal Asenuga, Idayat Titilayo Gbadamosi, Aduragbenro Deborah A Adedapo, Abimbola Obemisola Aro, Blessing Seun Ogunpolu, Fasilat Oluwakemi Hassan, Olufunke Olubunmi Falayi, Iyanuoluwa Omolola Ogunmiluyi, Temidayo Olutayo Omobowale, Oluwatosin Adetola Arojojoye, Olufunke Eunice Ola-Davies, Adebowale Benard Saba, Adeolu Alex Adedapo, Benjamin Obukowho Emikpe, Matthew Olugbenga Oyeyemi, Sanah Malomile Nkadimeng, Lyndy Joy McGaw, Prudence Ngalula Kayoka-Kabongo, Oluwafemi Omoniyi Oguntibeju, Momoh Audu Yakubu

Affiliations

  1. Department of Veterinary Physiology and Biochemistry, Faculty of Veterinary Medicine, University of Ibadan, Ibadan, Nigeria. [email protected].
  2. Department of Veterinary Medicine, Faculty of Veterinary Medicine, University of Ibadan, Ibadan, Nigeria.
  3. Department of Veterinary Pathology, Faculty of Veterinary Medicine, University of Ibadan, Ibadan, Nigeria.
  4. Department of Theriogenology, Faculty of Veterinary Medicine, University of Ibadan, Ibadan, Nigeria.
  5. Department of Veterinary Physiology and Biochemistry, Faculty of Veterinary Medicine, University of Benin, Benin, Nigeria.
  6. Department of Botany, Faculty of Science, University of Ibadan, Ibadan, Nigeria.
  7. Department of Pharmacology and Therapeutics, University of Ibadan, Ibadan, Nigeria.
  8. Department of Agriculture and Animal Health, College of Agriculture and Environmental Sciences, University of South Africa, Florida, South Africa.
  9. Department of Veterinary Physiology and Biochemistry, Faculty of Veterinary Medicine, University of Ibadan, Ibadan, Nigeria.
  10. Department of Veterinary Pharmacology and Toxicology, Faculty of Veterinary Medicine, University of Ibadan, Ibadan, Nigeria.
  11. Department of Biochemistry, Faculty of Sciences, Lead City University, Ibadan, Nigeria.
  12. Phytomedicine Programme, Department of Paraclinical Science, Faculty of Veterinary Science, University of Pretoria, Old Soutpan Road, Onderstepoort, Pretoria, 0110, South Africa.
  13. Phytomedicine and Phytochemistry Group, Oxidative Stress Research Centre, Department of Biomedical Sciences, Faculty of Health and Wellness Sciences, Cape Peninsula University of Technology, Bellville, Cape Town, 7535, South Africa.
  14. Department of Environmental & Interdisciplinary Sciences, College of Science, Engineering & Technology, Vascular Biology Unit, Center for Cardiovascular Diseases, Texas Southern University, Houston, TX, USA.

PMID: 33893992 DOI: 10.1007/s12011-021-02722-1

Abstract

Sodium fluoride (NaF) is one of the neglected environmental pollutants. It is ubiquitously found in the soil, water, and environment. Interestingly, fluoride has been extensively utilized for prevention of dental caries and tartar formation, and may be added to mouthwash, mouth rinse, and toothpastes. This study is aimed at mitigating fluoride-induced hypertension and nephrotoxicity with clofibrate, a peroxisome proliferator-activated receptor-alpha (PPARα) agonist. For this study, forty male Wistar rats were used and randomly grouped into ten rats per group, control, sodium fluoride (NaF; 300 ppm) only, NaF plus clofibrate (250 mg/kg) and NaF plus lisinopril (10 mg/kg), respectively, for 7 days. The administration of NaF was by drinking water ad libitum, while clofibrate and lisinopril were administered by oral gavage. Administration of NaF induced hypertension, and was accompanied with exaggerated oxidative stress; depletion of antioxidant defence system; reduced nitric oxide production; increased systolic, diastolic and mean arterial pressure; activation of angiotensin-converting enzyme activity and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB); and testicular apoptosis. Treatment of rats with clofibrate reduced oxidative stress, improved antioxidant status, lowered high blood pressure through the inhibition of angiotensin-converting enzyme activity, mineralocorticoid receptor over-activation, and abrogated testicular apoptosis. Taken together, clofibrate could offer exceptional therapeutic benefit in mitigating toxicity associated with sodium fluoride.

Keywords: Antihypertensive; Apoptosis; Cell signalling; Hypertension; Oxidative stress; Sodium fluoride toxicity

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