CC BY-NC-ND 4.0 · Ibnosina Journal of Medicine and Biomedical Sciences 2011; 03(05): 150-164
DOI: 10.4103/1947-489X.210888
Article

The impact of insulin-like growth factor-1, growth hormone, and oxidative stress in the experimental model of juvenile and adult hypothyroid retinal degeneration

Omyma Ahmed
1   Department of Physiology, Faculty of Medicine, Assiut University, Assiut, Egypt
,
Amal Taha
2   Department of Histology, Faculty of Medicine, Assiut University, Assiut, Egypt
,
Faten Mahmoud
3   Department of Anatomy, Faculty of Medicine, Assiut University, Assiut, Egypt
› Author Affiliations

Background: The pathophysiological mechanisms involved in hypothyroid retinal damage are still being debated. Materials and methods: Ninety-six pups of albino rats were equally divided into control, hypothyroid model and thyroid supplement groups. Each group was separated into juvenile and adult subgroups that were sacrificed at day 20 and 60 postnatally, respectively. Pups in the hypothyroid group were born to mothers who received 0.05 mg Carbimazole/day/pregnant female orally during gestation and at 20 days of lactation in juvenile subgroup. The adult subgroup received the hypothyroid agent until day 60 postnatally. The thyroid supplement group received antithyroid agent, then were treated with L-thyroxine orally (10 ug/kg body weight) for one month. Results: A significant reduction in body weight, temperature, heart rate, levels of Triiodothyronine (T3), Tetra-iodothyronine T4), growth hormone (GH) and Insulin-like growth factor (1GF-1), and antioxidant enzymes and an increase in systolic pressure and lipid peroxidation (LP) products were evident in hypothyroid subgroups associated with a decreasing thickness and degeneration of retina l layers. Thyroid supplementation group showed a partial normalization of the measured mediators accompanied by recovery of structural changes especially in the juvenile subgroup. Conclusions: Thyroid hormone has a vital role in normal retinal growth. GH, IGF-1 and oxidative stress are also significant mediators of retinal degeneration.



Publication History

Received: 23 January 2011

Accepted: 07 June 2011

Article published online:
23 May 2022

© 2011. The Author(s). This is an open access article published by Thieme under the terms of the Creative Commons Attribution-NonDerivative-NonCommercial License, permitting copying and reproduction so long as the original work is given appropriate credit. Contents may not be used for commercial purposes, or adapted, remixed, transformed or built upon. (https://creativecommons.org/licenses/by-nc-nd/4.0/)

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