Endoglin inhibition by sodium acetate and flutamide ameliorates cardiac defective G6PD-dependent antioxidant defense in gestational testosterone exposed rats

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dc.contributor.authorOlatunji, Lawrence Aderemi
dc.contributor.authorAreola, Emmanuel Damilare
dc.contributor.authorBadmus, Olufunto
dc.date.accessioned2025-05-07T12:30:40Z
dc.date.available2025-05-07T12:30:40Z
dc.date.issued2018-08-25
dc.description.abstractGestational androgen excess has been implicated in the development of cardiac dysfunction with poor me chanistic delineation. The role of sodium acetate on cardiac uric acid (UA) production and glucose-6-phosphate dehydrogenase (G6PD)-dependent antioxidant defense in pregnancy is not known. The study therefore sought to test the hypothesis that rats exposed to elevated testosterone in late pregnancy would have increased cardiac UA production and defective G6PD-dependent antioxidant defense. We also hypothesized that sodium acetate (SAc) or androgen receptor blocker, flutamide (Flu) would ameliorate these effects through endoglin inhibition. Twenty-four pregnant Wistar rats were treated (sc) with olive oil, testosterone propionate (0.5 mg/kg) singly or in combination with SAc (200 mg/kg; po) or Flu (7.5 mg/kg; po) in the late gestation between gestational day 14 and 19. The results showed that in the late gestation, testosterone exposure led to increased plasma and cardiac endoglin. In the heart of rats exposed to gestational testosterone there were elevated lactate dehydrogenase, adenosine deaminase, xanthine oxidase, uric acid (UA), cardiac injury markers and decreased G6PD-dependent antioxidant defense. However, either SAc or Flu comparably ameliorated these testosterone-induced effects. The data from the present study revealed that testosterone exposure in the late gestation causes elevated cardiac Eng that is accompanied by increased UA production and defective G6PD-dependent anti-oxidant defenses. Besides, the findings also suggest that the inhibitory effect of SAc or Flu on endoglin attenuates UA production and enhances the G6PD-dependent anti-oxidant barrier, thereby implying that endoglin may be a potentially novel therapeutic intervention for cardiac dysfunction particularly in pregnancy
dc.description.sponsorshipThis study was supported by the International Society of Hypertension (ISH) through the ISH grant for mentors (United Kingdom; 2017).
dc.identifier.citationOlatunji, L.A., Areola, E.D., & Badmus, O.O. (2018): Endoglin inhibition by sodium acetate and flutamide ameliorates cardiac defective G6PD-dependent antioxidant defense in gestational testosterone-exposed rats. Biomedicine and Pharmacotherapy, 107, 1641-1647, Published by Elsevier. Available online at: Biomedicine & Pharmacotherapy | Vol 107, Pages 1-1796 (November 2018) | ScienceDirect.com by Elsevier
dc.identifier.other10.1016/j.biopha.2018.08.133
dc.identifier.urihttps://uilspace.unilorin.edu.ng/handle/123456789/16358
dc.language.isoen
dc.publisherElsevier
dc.relation.ispartofseries107; 1641-1647
dc.subjectGestational androgen
dc.subjectEndoglin
dc.subjectG6PD-dependent antioxidant
dc.subjectHeart steatosis
dc.titleEndoglin inhibition by sodium acetate and flutamide ameliorates cardiac defective G6PD-dependent antioxidant defense in gestational testosterone exposed rats
dc.typeArticle

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