Indole-3 acetic acid induced cardiac hypertrophy in Wistar albino rats

• Published in: Toxicology and applied pharmacology Vol. 486; p. 116917
• Main Authors: Nayak, S.P. Ramya Ranjan, Boopathi, Seenivasan, Chandrasekar, Munisamy, Yamini, B., Chitra, Vellapandian, Almutairi, Bader O., Arokiyaraj, Selvaraj, Guru, Ajay, Arockiaraj, Jesu
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01-05-2024
• Subjects: Cardiotoxicity; Chronic kidney disease; Echocardiography; Plant growth regulator; Uremic toxin; Chronic kidney disease; Echocardiography; Plant growth regulator; Cardiotoxicity; Uremic toxin
• ISSN: 0041-008X; 1096-0333
• DOI: 10.1016/j.taap.2024.116917

Indole-3-acetic acid (IAA) is the most widely utilized plant growth regulator. Despite its extensive usage, IAA is often overlooked as an environmental pollutant. Due to its protein-binding nature, it also functions as a uremic toxin, contributing to its association with chronic kidney disease (CKD). While in vitro and epidemiological research have demonstrated this association, the precise impact of IAA on cardiovascular disease in animal models is unknown. The main objective of this study is to conduct a mechanistic analysis of the cardiotoxic effects caused by IAA using male Wistar albino rats as the experimental model. Three different concentrations of IAA (125, 250, 500 mg/kg) were administered for 28 days. The circulating IAA concentration mimicked previously observed levels in CKD patients. The administration of IAA led to a notable augmentation in heart size and heart-to-body weight ratio, indicating cardiac hypertrophy. Echocardiographic assessments supported these observations, revealing myocardial thickening. Biochemical and gene expression analyses further corroborated the cardiotoxic effects of IAA. Dyslipidemia, increased serum c-Troponin-I levels, decreased SOD and CAT levels, and elevated lipid peroxidation in cardiac tissue were identified. Moreover, increased expression of cardiac inflammatory biomarkers, including ANP, BNP, β-MHC, Col-III, TNF-α, and NF-κB, was also found in the IAA-treated animals. Histopathological analysis confirmed the cardiotoxic nature of IAA, providing additional evidence of its adverse effects on cardiovascular health. These results offer insights into the potential negative impact of IAA on cardiovascular function, and elucidating the underlying mechanisms of its cardiotoxicity.
•Serum Indole-3-Acetic Acid (IAA) concentration relevant to hemodialytic patients.•Echocardiogram reveals elevation of serum IAA leads to reduction of ejection fraction and fractional shortening.•IAA induces myocardial thickening in Wistar rats; elevated IAA led to dyslipidemia and oxidative stress.•Cardiac inflammatory biomarkers were over expressed in IAA-exposed rats.•IAA exposure led to cardiovascular damage and cardiac hypertrophy.