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Dysfunctional cardiac energy transduction, mitochondrial oxidative stress, oncogenic and apoptotic signaling in DiNP-induced asthma in murine model

Kehinde SA 1 , Olajide AT 2 , Fatokun TP 3 , Fouad D 4 , Hadi NR 5 , Elgazzar AM 6 Show all authors , James AS 7 , Ashour MHM 8

Affiliations 

  • 1 Biochemical Toxicology Laboratory, Faculty of Basic Medical Sciences, Ajayi Crowther University, Oyo, Nigeria. sa.kehinde@acu.edu.ng
  • 2 Cell and Signaling Laboratory, Department of Biomedical Science, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, Serdang, Malaysia
  • 3 Department of Drug Toxicology and Safety Pharmacology, Faculty of Life Sciences, University of Bradford, Bradford, UK
  • 4 Department of Zoology, College of Science, King Saud University, PO Box 22452, 11495, Riyadh, Saudi Arabia
  • 5 Department of Pharmacology and Therapeutics, Faculty of Medicine, University of Kufa, Kufa, Iraq
  • 6 Department of Forensic Medicine and Toxicology, Faculty of Veterinary Medicine, Alexandria University, Alexandria Town, Egypt
  • 7 Department of Neurosurgery and Brain Repair, Morsani College of Medicine, University of South Florida, Tampa, FL, USA
  • 8 Department of General and Pediatric Surgery, Faculty of Medicine, Tanta University, Second Tanta, Gharbia Governorate, Egypt
Naunyn Schmiedebergs Arch Pharmacol, 2025 Mar;398(3):2833-2843.
PMID: 39287675 DOI: 10.1007/s00210-024-03454-4

Abstract

Diisononyl phthalate (DiNP) has been associated with the development of allergies, asthma, and allergic airway inflammation. Through a complex interplay of signals and feedback mechanisms, the lungs communicate with the heart to ensure maintenance of homeostasis and supporting the body's metabolic demands. In the current study, we assessed the crosstalk between DiNP-induced asthma and cardiac cellular respiration, oxidative stress, apoptotic potential, and induction of oncogenic factors. Ten male BALB/c mice with a weight range of 20-30 g were divided into two groups, each comprising five mice. Group 1 (control), was administered saline orally for a duration of 30 days. In contrast, group 2 (DiNP group), received 50 mg/kg of DiNP to induce asthma. After the final administration and asthma induction, the mice were euthanized, and their hearts were excised, processed, and subjected to biochemical analyses. The DiNP group had downregulated (P 

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.

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