Affiliations 

  • 1 Department of Biomedical Science, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, 43400 UPM Serdang, Selangor, Malaysia
  • 2 Department of Ophthalmology, Faculty of Medicine, Universiti Kebangsaan Malaysia Medical Centre, 56000 Cheras, Kuala Lumpur, Malaysia
  • 3 Department of Pathology, Faculty of Medicine, Universiti Kebangsaan Malaysia Medical Centre, 56000 Cheras, Kuala Lumpur, Malaysia
  • 4 Centre for Eye Research Australia, Royal Victorian Eye & Ear Hospital, Melbourne, Australia; Ophthalmology, Department of Surgery, The University of Melbourne, Melbourne, Australia
  • 5 Department of Medical Microbiology and Parasitology, Universiti Putra Malaysia, 43400 UPM Serdang, Selangor, Malaysia; Genetics and Regenerative Medicine Research Center, Universiti Putra Malaysia, 43400 UPM Serdang, Selangor, Malaysia; Institute of Bioscience, Universiti Putra Malaysia, 43400 UPM Serdang, Selangor, Malaysia. Electronic address: sureshkudsc@gmail.com
  • 6 Tissue Engineering Centre, Universiti Kebangsaan Malaysia Medical Center, 56000 Cheras, Kuala Lumpur, Malaysia
  • 7 Department of Ophthalmology, Hospital Sultanah Aminah, 80100 Johor Bahru, Johor, Malaysia
  • 8 Department of Biomedical Science, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, 43400 UPM Serdang, Selangor, Malaysia; Department of Pharmaceutical Sciences, Irma Lerma Rangel College of Pharmacy, Texas A&M Health Science Center, Texas A&M University, College Station, TX 77843, USA
  • 9 Department of Biomedical Science, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, 43400 UPM Serdang, Selangor, Malaysia; Genetics and Regenerative Medicine Research Center, Universiti Putra Malaysia, 43400 UPM Serdang, Selangor, Malaysia; Department of Clinical Laboratory Sciences, College of Applied Medical Sciences, Jouf University, Sakaka, P.O Box 2014, Aljouf Province, Saudi Arabia. Electronic address: rachelmok2005@gmail.com
J. Photochem. Photobiol. B, Biol., 2019 Jul;196:111514.
PMID: 31154277 DOI: 10.1016/j.jphotobiol.2019.111514

Abstract

Retinal disorders account for a large proportion of ocular disorders that can lead to visual impairment or blindness, and yet our limited knowledge in the pathogenesis and choice of appropriate animal models for new treatment modalities may contribute to ineffective therapies. Although genetic in vivo models are favored, the variable expressivity and penetrance of these heterogeneous disorders can cause difficulties in assessing potential treatments against retinal degeneration. Hence, an attractive alternative is to develop a chemically-induced model that is both cost-friendly and standardizable. Sodium iodate is an oxidative chemical that is used to simulate late stage retinitis pigmentosa and age-related macular degeneration. In this study, retinal degeneration was induced through systemic administration of sodium iodate (NaIO3) at varying doses up to 80 mg/kg in Sprague-Dawley rats. An analysis on the visual response of the rats by electroretinography (ERG) showed a decrease in photoreceptor function with NaIO3 administration at a dose of 40 mg/kg or greater. The results correlated with the TUNEL assay, which revealed signs of DNA damage throughout the retina. Histomorphological analysis also revealed extensive structural lesions throughout the outer retina and parts of the inner retina. Our results provided a detailed view of NaIO3-induced retinal degeneration, and showed that the administration of 40 mg/kg NaIO3 was sufficient to generate disturbances in retinal function. The pathological findings in this model reveal a degenerating retina, and can be further utilized to develop effective therapies for RPE, photoreceptor, and bipolar cell regeneration.

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